Psychiatry Flashcards
Name endocrinological causes of dementia
- Hypothyroidism, Hyperparathyroidism, Cushing’s and Addisons
Name vitamin deficiency that causes dementia
B12, folate and thiamine
Metabolic causes of demenntia
- Hypoglycaemia, calcium, magnesium and electrolyte imbalance
Clinical features of dementia
- Memory impairment
- Personality changes
- Fatigue
- Apathy
- Hallucinations and paranoid delusions
- Sundowner syndrome
- Seizures
- Catastrophic Reaction
- Pathological emotion
Differentials of dementia
- Delirium
- Depression
- Learning Disability
- Normal ageing
Investigations for Dementia
- FBC; LFT; U&E; glucose; erythrocyte sedimentation rate (ESR); thyroid-stimulating hormone (TSH); calcium; magnesium; phosphate; Venereal Disease Research Laboratory (VDRL) test for syphilis; HIV; vitamin B12 and folate; C-reactive protein; blood culture; LP; EEG; chest X-ray (CXR); ECG; CT (optima and axial protocol); MRI; SPECT
Management of dementia
- Assessment
- Cognitive enhancement (Ach esterase inhibitors - rivastigmine), antioxidants (selegiline)
- Treat psychosis
- Treat depression
- Treat medical illness
- Psychological support to patient and care-givers
- Functional management: maximise mobility, encourage indépendance
- Social management
What is catastrophic reaction
Happens when patients with dementia are asked to perform tasks that they are struggling with causing sudden anger, agitation and violence
What characterises fronts-temporal dementia
- Frontal lobe so personality changes are early
2. Language impairment
Onset of front-temporal dementia
Early-onset
What would a CT show for fronts-temporal dementia
- Atrophy of fronto-temporal cortex
What would a SPECT show for fronto-temporal dementia
fronto-temporal metabolism
What part of the cortex does alzheimer’s affect
Posterior-parietal
What characterises alzheimer’s
- Early memory and cognitive deficits
personality changes are later as frontal lobe starts to atrophy
Most common cause of dementia
Alzheimer’s
What can protect against Alzheimer’s
Smoking
Oestrogen
NSAIDs
What causes Alzheimer’s
- Amyloid plaques (beta-amyloid deposits)
2. Neurofibrillary tangles
Clinical symptoms of alzheimer’s (related to time)
Early symptoms: Memory problems, ADL issues, spatial dysfunction and changes to behaviour (e.g. irritability)
Middle: Intellectual and personality deterioration (aphasia, apraxia so struggling to dress) and agnosia (can’t recognise own body parts)
Impaired visuospatial skills
Late: Fully dependant with physical deterioration, incontinence, weight loss, primitive reflexes and extrapyramidal signs
Psychiatric symptoms of alzheimer’s
- Paranoid Delusions, auditory and visual hallucinations, depression
Factors for poor prognosis of alzheimer’s
- Sveerity of presentation
- Male
- <65
What assessment is used for Alzheimer’s
IQCODE
What imaging would be used for alzheimer’s
- CT: Cortical atrophy
- MRI: Atrophy of grey matter (hippocampus and amygdala)
- PET: 20-30% reduction in oxygen
How often should patients be reviewed if they are put on treatment for alzheimer’s
Every 6 months
MMSE should be above 12 to continue treatment
What drugs are given to patients with Alzheimer’s
- Donepezil or Rivastigmine
2. Memantine
Side-effect of AChEIs
GI bleeding
How does Memantine function
- NMDA-receptor antagonist which protects over-excitation of neurons.
Clinical features of Lewy-Body Dementia
- Dementia
- Parkinsonism
- Fluctuating cognitive performance
- Complex Hallucinations
- Depression
- Transient episodes of consciousness disturbances (mute and unresponsive for several minutes)
How long does it take to rapidly deteriorate from lewy body
1-2 years
Name two of three core features that are needed to diagnose lewy body
- Fluctuating cognition with variation in alertness and attention
- Recurrent visual hallucinations
- Spontaneous motor features of parkinsonism
When is Lewy Body less likely to be diagnosed
Presence of a stroke
Pathology of lewy body
- Phosphorylated neurofilament proteins with ubiquitin and A-synuclein
These deposit in substantial nigra and hippocampus
Differentials of lewy body
- Delirium
- Mania, depressive disorder
- Parkinson’s
Investigations of lewy body
- CT/MRI
2. SPECT
What is seen in CT/MRI in lewy body
deep white matter lesions and periventricular lucencies on MRI
Sparing of medial temporal lobes
How is Lewy Body treated
- Antipsychotics, AChEIs
Core features of FTD
- Gradual progression
- EARLY decline in social interpersonal conduct
- EARLY impairment in regulation of social conduct
- EARLY emotional blunting
- EARLY loss of insight
Supportive: Dietary changes (e.g. overeating, preferring sweet food) Speech disturbances (e.g. mutism and echolalia)
Progressive symptoms: Primitive reflexes, Parkinsonism, MND
Investigations of FTD
- EEG should be normal despite evident dementia
2. Brain imaging
Pathology of FTD
Macroscopic: 1. Bilateral atrophy of frontal and anterior temporal lobes
Microscopic: loss of cortical nerve cells and spongiform degeneration
Pick: loss of large cortical nerve cells, no spongiform change, swollen neurones, widespread gliosis
Three main features of vascular dementia
- Cognitive deficits following a single stroke
- Multi-infarct dementia (from multiple strokes)
- Progressive small-vessel disease
Clinical Features of vascular dementia
- EARLY emotional and personality changes followed by cognitive deficits that fluctuate
- Depression and sundowner syndrome
- Neurological impairments
Investigations of Vascular dementia
- Routine screen
- Serum Cholesterol, clotting and vasculitis screen (ESR, CRP and RF, Anti DsDNA, APL), syphillis if young
- ECG, CXR, CT and MRI ESSENTIAL
Management of vascular
- Establish causative factors.
- Medical or surgical diseases that are contributory need to be treated early.
- Daily aspirin may delay course of disease.
- General health interventions include changing diet, stopping smoking, managing hypertension, optimizing diabetic control, and increasing exercise.
Pathology of neurosyphilis
- Spirochaetes go for frontal and parietal lobes and presents as progressive frontal dementia
Symptoms: Grandiosity, euphoria and mania
Tremor, Ataxia and trombone tongue
Pathology of Huntington’s
Triad repeat of CAG between 37 and 120 on chromosome 4
This decreases GABA neutrons in basal ganglia -> increased stimulation of thalamus and cortex of global pallid us.
Clinical features of huntington’s
TRIAD:
- Chorea (jerks, tics and involuntary movements of ALL parts of the body, grimacing, dysarthria and positive primitive reflexes, abnormal eye movement)
- Dementia
- History of HD
Psychiatric:
Anxiety and depression
Psychosis
Agression and violence
What does a CT/MRi show for huntington’s
- Atrophy of Basal Ganglia
Features of substance misuse dependance syndorme
- Drug seeking behaviour
- Increased tolerance to drug effects
- Loss of control of consumption
- Signs of withdrawal
- Signs of withdrawal
- Drug taking to avoid withdrawal symptoms
Stages of change
- Pre-contemplation (user doesn’t recognise problem)
- Contemplation
- Decision
- Action
- Maintenance
- Relapse
How do we screen for alcohol problems
CAGE
AUDIT and FAST assessment papers
Blood tests in heavy drinkers
MCV (raised)
GGT raised
CDT
Recommended units for men and female
- 21 - Men
- 14 - Female
Should be at least 2 days a week of non-drinking
Techniques of controlled drinking
- Pricing
- Motivational interview
- Counselling families
What is uncomplicated alcohol withdrawal syndrome
How long does this last
- Coarse tremor, sweating, insomnia, tachycardia and anxiety
- Transient hallucination
- Craving for alcohol
48Hours
When do withdrawal symptoms occur
4-12 hours after last drink
Onset of delirium tremens
1-7 days after drink, 48Hours usually
Clinical features of delirium trmeens
- Uncomplicated withdrawal symptoms
- Disorientation
- Loss of conscious
- Amnesia
- Hallucinations
- Paranoid delusions
Differentials of delirium
- Hepatic encepholapath y
2. Head Injury
How is alcohol withdrawal managed
- BDZ to manage tremor and anxiety
- Antipsychotics
- Dilsufiram (irreversible inhibition of Acetaldehyde Dehydrogenase which converts alcohol to water and co2)
- Acamprosate (anticraving)
Name two types of alcohol-induced amnesia
- En bloc - Well demarcated start and finish points
2. PartialL Episodes of island episodes which have been forgotten
Alcohol can cause Othello syndrome, what is this
Mono symptomatic Paranoid delusion disorder
What is Wernicke’s encephalopathy
- Acute onset of:
Acute confusional state
opthalmoplegia, nystagmus
ataxic gait
CAUSED: Thiamine deficiency
How is Wernicke’s encephalopathy treated
- IV Thiamine
2. ALL should have parenteral vitamins
How long can wernicke’s last untreated
72 weeks
What is Korsakoff’s syndrome
- Retrograde amnesia
2. But has working memory
How is korsakoff’s syndrome treated
- Oral thiamine
- Vitamin supplement
- Treat psychiatric comorbidity
Medical complications of alcoholic misuse
- ALD
- Gastritis, Barrett’s, Malloryy-weiss tears, peptic ulcers, chronic pancreatitis
- HTN, Dilated cardiomyopathy, CVA
- TB, Strep pneumonia
- Central pontine myelinolysis, optic atrophy, ceberellar degeneration
- Erectile problems, hypogonadism
- Gout, osteoporosis, Foetal alcohol syndrome
How do you assess the drug user
- Background
- Reason for consult
- Current drug use
- Lifetime drug use
- Complication
- Precious treatment
- Medical and psych history
- Fam
- Social
- Forensic
- Patient aims
- MSE
- Physical
- Urine screening essential
Symptoms of opiate withdrawal
- Sweating
- Dilated pupils
- Tachy cardia
- Hypertension
- Piloerection
VOMITING - Tremor and diarrhoea
What is given for opiate withdrawal
- Lofexidine (alpha-adrenergic agonist)
2. Methadone or Buprenophine
Symptoms of BDZ withdrowal
- Anxiety
- Insomnia
- Tremor
- Agitation
- Headache
- Seizures
How are BDZ symptoms treated
Smallest dose of diazepam that stops symptoms
Then dose is reduced
How is Schizophrenia diagnosed
AT LEAST ONE OF THE FOLLOWING:
- Thought echo, insertion, withdrawal or broadcasting
- Delusions of control, influence or passivity; clearly referred to body and limb movements
- Hallucinatory voices
- Persistent delusions
AT LEAST TWO OF THE FOLLOWING:
- Persistent hallucination
- Catatonic behaviour
- Negative symptoms
- Consistent change in behaviour
More than a month
What substances can induce shizocphrenia type symptoms
- Alcohol
- Stimulants
- Steroids
- Antihistamines
What causes schizophrenia
- Dopaminergic hyperactivity
- Glutaminergic hyperactivity
- Serotenergic overactivity
Why is there a 20% reduction in life expectancy with people having schizophrenia
Suicide
Which family members are most affected for schizophrenia
Twins
Investigations for schizo
- Routine blood tests
- CT or MRI if neurological deficits found
- CXR if comorbid respiratory etc
- Urine for drug screen
- EEG if history of seizures
Special: 24-hr collection for cortisol
24hr catecholamine for phaeochromotocytoma
Stage of schizophrenia
- Prodromal state (non-specific, negative symptoms)
- First episode where there is a direct event related to their condition
- Relapse and re-starting subsequent episodes
How is prodrome stage assessed
PACE
How is acute psychosis treated
- Rispiridone
2. Long acting BDZ to control behavioural disturbances
Extra-pyramidal effects of antipsychotics
Typical and atypical both cause them but less so with atypical:
- Dystonias
- Parkinsonism
- Akathisia
How is parkinsonism treated
Procyclidine
How should negative symptoms be treated
Mood medications
How can the effect of clozapine be enhanced
SSRI, lamotrigine or second antipsychotic
What is the first stage of discharge planning
- CPA
What should be done if oral medications are refused
- Depot injections
What types of psychological therapies can reduce relapse
Family therapy and psychoeducation
What assessments should be made at every schizo check up
- MSE
- Side-effects to drugs
- Recent life stresses
What advice would I give to a schizo patient
- Provide education on disease and treatment
- Concerns adressed
- Offer to meet family members
What type of injections are depots for antipsychotics
IM
Benefits of atypical psychotics
- Less likely to cause extra pyramidal side effects
What receptor does rispiridone act on
5-HT2
To avoid sedation what drug should be given
- High potency (haloperidol) or non-sedating (risperidone)
To avoid weight gain what drug should be given
- Haloperidol or fluphenazine
What antipsychotics cause postural hypotension
Phenothiazides
EPSE examples
- Acute dystonia (where contraction of muscle groups to maximal limit)
- Parkinsonism (tremour, rigidity and bradykinesia)
- Akathisia (restlessness of lower limbs)
- Tardive dyskinesia (athetosis and chorea of mouth)
How is acute dystonia treated
Parenteral procyclidine
How is TD treated
VIT E helps deterioration
Anticholingeric sideeffects
- Dry Mouth
- Blurred vision
- Urinary retention
- Constipation
- Glaucoma
Anti-adrenergic side-effects
- Postural hypotension
- tachycardia
- Sexual dysfunction
Antihistaminic side effects
- Sedation
2. Weight gain
Before considering treatment resistant schizo, what factors do we need to think about
- Drug non compliance
2. Lack of adequate treatment or contraindications
How is TRS managed
- Diagnosis clarified
- See if comorbid substance misses is occurring
- Psychoeducation for noncompliance
- Clozapine or depot
When is clozapine prescribed to schizo patients
- If patient with schizo has not adequately responded to treatment
Pharmacology of clozapine
- Blocks D1 and D4 receptors
Side effect of lithium
Lowers threshold for seizures
Side-effects of clozapine
- Constipation, fever, hyper salivation, hypertension, hypotension, nausea, agrunlocytosis, nocturnal enuresis, sedation, seizures, weight gain
Main two depot medications
- Haloperidol and risiridone
What is post-injection syndrome
- Immediate sedation, ESPEs, basically side effects after depot injection
What is schizoaffective disorder
• An uninterrupted period of illness during which there is a major depressive, manic, or mixed episode concurrent with symptoms that meet criterion A for schizophrenia.
How long before schizoaffective disorder can be diagnosed
2 weeks
What is Schizotypal disorder
- CLUSTER A PD
Clinical features of achizo without delusions or hallucinations
e.g. Ideas of reference (you guys are talking about me), Social anxiety, odd beliefs and magical thinking , odd speech
Differential for schizotypal
- Autism, asperger;s, PD cluster A
how is schizotypal disorder treated
- Rispiridone
What is schizophreniform disorder
- schizophrenia like psychosis that can’t be classified as schizo
What is De Clerambault syndrome
- Person believes that someone if in love with them
What is persecutory syndrome
- Patients believe someone wants to harm them
Risk factors for schizophreniform
- Social isolation
3. Low socio economic status
Definition of acute psychotic disorder
- Sudden onset, variable presentation (including perplexity, inattention, formal thought disorder/disorganized speech, delusions or hallucinations, disorganized or catatonic behaviour), usually resolving within less than 1mth (DSM-5) or 3mths (ICD-10).
Differentials of acute psychotic disorder
- organic disorders
- BAD
- Drugs and alcohol
What is folie a deux disorder
Shared delusions
What causes foil a deux disorders
- Psychodynamic (where people feel like they will lose the other partner if they do not share beliefs)
- Learning theory
- . Social isolation
How is folly a deus managed
- Separation
What is Capgras delusion
- the patient believes others have been replaced by identical or near identical imposter
What is fregoli syndrome
- an individual, most often unknown to the patient, is actually someone they know ‘in disguise’.
What is inter metamorphosis delusion
- the patient believes they can see others change (usually temporarily) into someone else (both external appearance and internal personality).
What is subjective doubles delusion
the patient believes there is a double (‘dopplegänger’) who exists and functions independently.
What is autoscopic syndrome
the patient sees a double of themselves projected onto other people or objects nearby.
What is reverse fregoli syndrome
the patient believes others have completely misidentified them.
Core symptoms of depression
- Depressed mood
- Loss of interest
- Weight change
- Disturbed sleep
- Psychomotor agitation
- Fatigue
- Loss of libido
- diminished concentration
- Recurrent thoughts of death
What is anhedonia
Loss interest in things
Biological symptoms of depression
- Anhedonia
- Loss of appetite
- Loss of weight
- Loss of libido
Psychotic symptoms
- Delusions
- hallucinations
Depressive stupor (lack of mental function)
What is non-melancholic depression
- Irritable or hostile depression
- Anxious depression (shy and withdrawn)
No somatic (biological) symptoms
What is melancholic depression
Has biological symptoms
Where is depression more common
Female, young Marital status Adverse life events Physical illness Low socio-economic status
Structural brain changes in depression
- Ventricular enlargement
- Sulcal prominence
- Hypoperfusion in frontal, temporal and parietal areas.
Assessment of depression
- HAM-D scale
- Check co-morbidity of anxiety with HAM-A
- MMSE
Investigations ofr depression
- Blood tests
- Urine
- Breath
- ABG
- Thyroid antibodies
- Antinuclear antibody
- Ayphilis serology
- Dexamthesone suppression test
- Cosyntropin stimulation test (addison)
- Lumbar puncture
Poor prognosis of depression
- Lack of support social
2. Low self confidence
When should patients on antidepressants be followed up
- 1-4 weeks
When should ECT for depression be considered
- Severe biological symptoms
2. First line for depression with psychotic symptoms
How should SSRIs be discontinued
- Gradually half the dose over months
First line treatment for psychotic depression
- Olanzapine and fluoxetine
Problems with dual combination in psychotic depression
- Antipsychotic can mask improvement on SSRI
2. Combination may worsen side-effects
Treatment resistant depression management
- Is diagnosis correct, conduct more blood tests
- Check compliance
- Consider change in antidepressant
- ECT?
TRYPTOPHAN
Atypical depressive features
- Depressed but reactive to experiences
- Hypersomnia
- Hyperphagia
- Leaden paralysis
- Oversensitivity to rejection
- Initial insomnia than early morning awakening
How is atypical depression treated
PHENELZINE (MAO inhibitor)
How is SAD treated
- Light Therapy
2. SSRI
What is Dysthymic disorder
- PD
Clinical features of dysthymic disorder
- Depressed mood
- Reduced appetite or increased
- Changes in sleep
- Low self esteem
- Poor conc
- Difficulties making decision
How does switching MAO medication differ from other drugs
MAO needs a washout period whereas cross-taper is usual for others.
Side-effects of MAOIs
- Hypertensive crisis as intestinal MAO are inhibited
2. Dietary tyramine needs to be avoided
Side-effects of SSRIS
- Agitation, GI upset, nausea, diarrhoea and headache as it affects 5-HT3 agonism
Side effects of SNRIs
- Nausea, GI upset, constipation, loss of appetite, sweating, headache and sexual dysfunction
Name types of SNRIs
- Vanlafaxine
2. Duloxetine
Sid effects of Tetracyclic antidepressants
- GI issues
Name a Serotonin antagonist reuptake inhibitor
- Trazodone
Mode of action of SARIs
- 5-HT1A/1C/2Aantagonism—sedating/anxiolytic, less sexual dysfunction;
- 5-HT agonism through the active metabolite (m-chlorophenylpiperazine)—antidepressant effect;
- α1 antagonism—orthostatic hypotension;
- H1antagonism—sedation and weight gain.
Side effect of mirtazepine
- Increase in appetite
2. Weight gain
What type of antidepressant is mirtazapine
- Noradrenergic and specific serotonergic antidepressant
Name a noradrenaline reuptak inhibitor
- Reboxetine
What type of antidepressant is Bupropion
Noradrenergic and dopaminergic reuptake inhibitor
Indications for ECT
- Depression, Treatment resistant psychosis and mania, catatonia, neuroleptic malignant syndrome, seizures
Side-effects of ECT
transient memory loss, seizures
Tonic contraction
Increase in cortisol
Raised ICP
Retrograde amnesia Long-term emory loss Confusion Muscular aches Clumsiness
Things to do before ECT is carried out
- Patient fasts for 8 hours
- establish IV access, oxygen mask, muscle relaxant
- Hyperventilation
How is ECT carried out
- Apply electrodes to scalp
- Test for contact between electrodes and scalp
- Monitor length of seizure
Types of ECT
Unilateral ECT and BECT
How often does ECt hav to be carried out
- Twice a week
6-12 for depression
catatonic in 3-5
If ECT is causing prolonged seizures how is this treated
- Administer IV diazemuls every 30s
Surgical methods for depression
Vagus nerve stimulation
Deep brain stimulation
What medications can INDUCE mania
- Anti-depressants
- BDZ
- Lithium
- DIsulfiram
- Anti-parkinsonian
- Propanolol
- Opioids
- Steroids
Clinical features of mania
- Elevated mood
- Increased energy (either over activity or reduced need for sleep)
- Though disorder (Pressured speech, flight of ideas, racing thoughts)
- Increased self-esteem (grandiosity, reduced social inhibition, over familiarity)
- Reduced attention
- Behaviours which can cause serious consequences
Agression, irritability
Psychotic symptoms of mania
- Grandios
- Suspiciousness
- Pressured speech to point where they can’t communicate
- Flight of ideas, proximity
- Irritation and aggression
- Catatonic features (Manic stupor)
- Loss of insight
Differentials of mania
- Anxiety
- PTSD
- ADHD
- Schizophrenia
- Alcohol misuse
How is mania managed
- Risk assessment and ensure safety
- Exclude other causes
- Address any specific psychosocial stressors
Hypomania Clinical features
- Mild elevation of mood
- Increased energy
- Increased self-esteem
- Sociability
- Talkativeness
- Over-familiarity
- Increased sex drive
- Reduced need for sleep
- Difficulty in focusing on one task alone
Differential diagnosis of hypomania
- OCD
- Substance misuse
- Physical illness
Characteristic Clinical features of bipolar spectrum disorder
- AT LEAST one depressive episode
- No spontaneous hypomanic or manic episodes
The history will include some of the following:
- A family history of bipolar disorder in a first-degree relative.
- Antidepressant-induced mania or hypomania.
- Hyperthymic personality2 (at baseline, non-depressed state).
- Recurrent major depressive episodes (>3).
- Brief major depressive episodes (on average, <3mths).
- Atypical depressive symptoms (DSM-IV criteria).
- Psychotic major depressive episodes.
- Early age of onset of major depressive episode (
Treatment of bipolar disorder
- Lithium/Valproate and SSRI
Why is SSRI not typically used for bipolar
- Causes rapid cycling
Bipolar diagnostic threshold
- AT least TWO episodes of mania and unipolar depression
What type bipolarism is associated with substance and medication use
- Type 2
What type bipolarism is associated with other medical conditions
Type 2
Main differences between type 1 or 2
Type 2 is mainly hypomanic , more episodes of depression
Type 1 is mainly mania with or without depression
There is also mixed
Investigations for bipolari
As for depression; full physical and routine blood tests to exclude any treatable cause, including FBC, ESR/CRP, glucose, U&Es, Ca2+, TFTs, LFTs, drug screen. Less routine tests: urinary copper (to exclude Wilson’s disease [rare]), ANF (SLE), infection screen (VDRL, syphilis serology, HIV test). CT/MRI brain (to exclude tumour, infarction, haemorrhage, MS)—may show hyperintense subcortical structures (esp. temporal lobes), ventricular enlargement, and sulcal prominence; EEG (baseline and to rule out epilepsy). Other baseline tests prior to treatment should include ECG and creatinine clearance.
Poor prognosis of bipolar disorder
- poor employment history; alcohol abuse; psychotic features; depressive features between periods of mania and depression; evidence of depression; male sex; treatment non-compliance.
Good prognosis of bipolar disorder
manic episodes of short duration; later age of onset; few thoughts of suicide; few psychotic symptoms; few comorbid physical problems, good treatment response and compliance.
How are catatonic symptoms (manic stupor) treated
- ECT or BDZ with Lithium
How is acute mania treated
- Lorazepam and haloperidol (low-dose antipsychotics)
If patient is already on prophylaxis for bipolarism, what do we need to do
- Check serum levels
- Exclude other problems
- Consider adding SSRI to mood-stabiliser
- OR if not already on antipsychotic, add quetiapine
If recent mood instability isn’t helped by lithium what is 2nd line treatment
Lamotrigine
1st line for life threatening depressive episode
ECT
Non-medical interventions for bipolar
- Psychoeducation
- CBT
- Family focused therapy
- Interpersonal and social rhythm therapy
Cyclothymia clinical features
Rapid cycling, mood swings
Treatment of cyclothymia
- Lithium low-dose, carbamazepine
2. At crisis, treat with low dose antipsychotic
How is Lithium monitored
- Thyroid function
- eGFR
- Blood serum levels (FBC, U and E)
When should lithium levels be checked
5 Days after starting, 5 days after dose change
Then every 3 months
How is lithium stipped
Gradually reduced
Side-effects of lithium
- Polyuria, Marked tremor, anorexia, nausea/vomiting, diarrhoea (sometimes bloody), with dehydration and lethargy.
- Kindey interstitial fibrosis, Hypothyroidism, teratogenicity
- T-waves change and QRS widens
When is valproateindicated
- Acute mania
- Acute depressive episode
- Prophylaxis of bipolar affective disorder
Side-effects of valproate
- Gi Upset, raised LFTs, tremor, sedation.
When is carbamazepine indicated
- Acute mania
- Acute depressive episode
- Prophylaxis of bipolar
What is psychoeducation
- Patients are given a theoretical and practical approach to understand their illness and the medication they are prescribed. Through understanding, patients can attain improved adherence to medication, recognize symptoms that might lead to decompensation, and recover occupational and social function.
What is CBT
- TIME-LIMITEd but focused education on condition and teach cognitive behavioural skills to cope with stressors
What is Interpersonal and social rhythm therapy
- to reduce lability of mood by maintaining a regular pattern of daily activities, e.g. sleeping, eating, physical activity, and emotional stimulation.
What is family-focused therapy
usually brief, includes psychoeducation (of patient and family members) with specific aims: accepting the reality of the illness, identifying precipitating stresses and likely
Describe schizoid PD
- Emotionally cold, detachment, lack of interest in others, excessive introspection and fantasy.
Describe Emotionally unstable–impulsive type
Inability to control anger, or plan with unpredictable behaviour
Describe Emotionally unstable–borderline type
Unclear identity, intense and unstable relationships, unpredictable affect, threats or acts of self-harm, impulsivity.
Describe Histrionic PD
Self-dramatization, shallow affect, egocentricity, craving attention and excitement, manipulative behaviour.
What are risk factors for Cluster B PDs
- Substance Misuse
- Easting Disorder
- Somatoform disorders
4
Risk factors for cluster B PD
- Eating Disorder
- Neurotic disorder
- Depression
How is PD assessed
SELF-REPORT QUESTIONNAIRE: PDQ-IV
INTERVIES: SCID-5-PD
How is OCD treated
SSRI
Psychotherapy for borderline
DBT
Or Cognitive analytic therapy
What is Hyperventilation Syndrome
- Ventilation exceeds metabolic demands, leading to haemodynamic and chemical changes producing characteristic symptoms (dyspnoea, agitation, dizziness, atypical chest pain, tachypnoea, hyperpnoea, paraesthesias, and carpopedal spasm) usually in a young, otherwise healthy patient. HVS relatively common presentation; may be mistaken for panic disorder. Considerable overlap, hence inclusion here:
Clinical Features of HVS
- Chest pain/angina
- Tachypnoea, dyspnoea and wheeze
- CNS (hypocapnia): Dizziness, weakness, paraesthesias, visual hallucinations
- GI: Bloating, flats, epigastric pressure
Investigations for HVS
- Routine blood tests
- ABG
- Pulse oximetry
- PaCO2, HCO3 - low
- CXR
How is HVS treated
- Reassure patient
- Use BDZ for severe anxiety
- Establish normal breathing pattern
Education
Beta-blockers, BDZ prophylaxis
Define a panic attack
eriod of intense fear characterized by a constellation of symptoms (see Box 9.1) that develop rapidly, reach a peak of intensity in about 10min, and generally do not last longer than 20–30min (rarely over 1hr)
Define a panic disorder
Recurrent panic attacks, which are not 2° to substance misuse, medical conditions, or another psychiatric disorder.
Clinical features of panic attack
- Palpitations, pounding heart, or accelerated heart rate.
- Sweating.
- Trembling or shaking.
- Sense of shortness of breath or smothering.
- Feeling of choking or difficulties swallowing (globus hystericus).
- Chest pain or discomfort.
- Nausea or abdominal distress.
- Feeling dizzy, unsteady, light-headed, or faint.
- Derealization or depersonalization (feeling detached from oneself or one’s surroundings).
- Fear of losing control or going crazy.
- Fear of dying (angor animus).
- Numbness or tingling sensations (paraesthesia).
- Chills or hot flashes.
How are panic disorders managered
- Citalopram
- BDZs: Lorazepam
2nd line use BDZs
CBT
Psychodynamic psychotherapy
Define agoraphobia
Anxiety and panic symptoms associated with places or situations where escape may be difficult or embarrassing (e.g. of crowds, public places, travelling alone or away from home), leading to avoidance.
How are phobias managed
- Exposure therapy
2. Severe: BDZs
Management of social anxiety
CBT and SSRI/beta blockers
Define GAD
‘Excessive worry’ (generalized free-floating persistent anxiety) and feelings of apprehension about everyday events/problems, with symptoms of muscle and psychic tension, causing significant distress/functional impairment.
How is GAD amanged
- CBT but less affective in these cases
Psychotic symptoms: Busprione
Somatic: BDZz
Depressive: SSRI
CV: Beta blockers
WORST CASE: Psychosurgery
Define OCD
A common, chronic condition, often associated with marked anxiety and depression, characterized by ‘obsessions’ (see Anxiety and stress-related disorders [link]) and ‘compulsions’ (see Anxiety and stress-related disorders [link]).
Psychological management of OCD
- CBT
2. Behavioural or cognitive therapy
If OCD becomes severe what must be considered
- ECT, psychosurgery
DBS but not benefit established
Define hoarding disorder
Persistent difficulties in discarding or parting with possessions (including pets), regardless of their actual value, which leads to distress associated with discarding them and results in the accumulation of possessions that clutter active living areas.
Denis type 1 trauma
single, dangerous and overwhelming events comprising isolated (often rare) traumatic experiences of sudden, surprising, devastating nature, with limited duration.
Define type 2 trauma
due to sustained and repeated ordeal stressors