PSYCHIATRY Flashcards
Describe the aetiology of ADHD.
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
What are the 3 core behaviours of ADHD?
- Hyperactivity.
- Inattention.
- 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
ADHD core behaviours: give 3 signs of impulsivity.
- Blurts out answers.
- Interrupts.
- Difficulty waiting turns.
- When older, pregnancy and drug use.
ADHD core behaviours: give 3 signs of inattention.
- Easily distracted.
- Not listening.
- Mind wandering.
- Struggling at school.
- Forgetful.
- Organisational problems.
Does not appear to be listening when spokento directly
Makes careless mistakes
Looses important items
What is the diagnostic criteria for ADHD? According to DSM-5 (Diagnostic and Statistical Manual of Mental Disorders)
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
.
What are some differentials of ADHD?
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).
What tools can be used in order to diagnose ADHD?
- Clinical interview - are there any RF’s for ADHD?
- ADHD nurse classroom observation.
- Questionnaires (SNAP), Conor’s questionaire
- Quantitative behavioural (QB) analysis.
Brown attention deficit disorder scale
WHO adult ADHD self-report scale
Describe the nn pharmalogical treatment for ADHD.
- Education.
- 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
What are some medicine for ADHD?
Methylphenidate (ritalin, concerta, Equasym)
Atomoxetine (Strattera®) A non-stimulant NE reuptake inhibitor licensed for the treatment of ADHD.
What are some things you need to consider/ SE of ADHD medication?
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
What are the 3 main features of the deficits seen in ASD?
They can be categorised as deficits in social interaction, communication and behaviour
Outline some social interaction issues often seen in those with ASD
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
Outline some communication issues often seen in those with ASD
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
Outline some behavioural issues seen in Autism
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
Describe the treatment for ASD.
- 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..
Outline some of the people within the MDT for dealing with ASD.
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
What are some risk factors for depression?
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)
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?
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).
What are some things you may find on consulation/examination/investigations for depression?
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
What is the name of the questionaire used in depression?
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
What is the non pharmalogical measurements for mild depression?
aka PHQ-9 less than 15
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
What is the treatment for moderate/severe depression? aka PHQ-9 of more than 15 - How long for remission of symptoms before tapering off?
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
What is some treatment for very severe depression
Resistant depression Tx w/ combo of antidepressants +
Lithium
Atypical antipsychotic
Another antidepressant
ECT very effective in severe cases (Electroconvulsive Therapy)
Outline what bipolar disorder consists of - what is the ICD-10 definition
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
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
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)
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
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
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
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
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
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
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.
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
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
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
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
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
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
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
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
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
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)
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
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
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.
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
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
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.
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
What is seen in postpartum psychosis?
Postpartum psychosis – 1-2:1000
Depression
Mania
Psychosis
What is the treatment of puerperal psychosis?
Admission to the mother and baby unit
Cognitive behavioural therapy
Medications
Electroconvulsive therapy (ECT)
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.
Define PTSD
Post traumatic stress disorder
Develop (immediately/delayed) post exposure to stressful event/threatening, catastrophic situation
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
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
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
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)
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
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
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
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)
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
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
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.
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
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
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
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
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
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
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.
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
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.
Schizophrenia and psychosis - define delusions
Delusions: a fixed, false belief not in keeping with cultural and educational background.
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.
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
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
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
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)
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).
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
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
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
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
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
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
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)
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
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
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
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
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
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
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
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
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.
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
What are some signs seen in conversion disorders?
paralysis
Loss of speech
Sensory loss
Seizures
Amnesia
Examination and investigations are inconsistent
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.
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
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
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.
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)
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”
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)
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).
Give some specific persoanility disorders group in Cluster A personalty disorder
Paranoid
Schizoid
Schizotypal
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
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
SchizoiD - = Distant
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
SchizoTypical -
magical thinking
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
What are the personality disorders grouped together in Cluster B?
Bad
borderline (emotioanlly unstable)
antisocial,
histrionic
narcissist,
BAHN
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?
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
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
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
Name some other conditions that are thought to have a genetic link with personality disorders seen in Cluster B?
Depression
Bipolar
Substance abuse disorder
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
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
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,
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
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
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
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
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
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
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!!
Name 3 broad kinds of psychological therapies
1 Supportive therapy
Explorative pyschotherapies=
2 Cognitive and Behavioural therapies
3 Psychodynamic therapies
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.
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
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!!!!!!
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
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.
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).
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
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
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
What are some symptoms of opiate overdose
Acute presentation = drowsiness
Respiratory depression -> resp acidosis CO2 retention)
Hypotension
Tachycardia
Pinpoint pupils
Chronic = constipation
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.
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
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
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
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
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.
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
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).
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
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
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…
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.
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
