General Adult Psychiatry Flashcards
DIS
Diagnostic Interview Schedule
1981 Robins
Structured diagnostic interview designed for use by lay interviewers
ECA programme
NIMH
Epidemiological Catchment Area Programme
CIDI
WHO Composite International Diagnostic Interview
Version of DIS that used ICD criteria
NCS
National Comorbidity Survey
First to use the CIDI. 1990-2.
8000 respondents
Reinterviewed between 2000-1 - called NCS-R
Found substantially higher prevalence results than the ECA
Most prevalent anxiety disorder was specific phobia.
Findings of ECA and NCS
Number of people with MH problems far outweighed resources available
Did not comment on severity therefore likely overstated demand
WMH-CIDI
Revised version of CIDI
Assesses severity and other aspects such as risk factors, socio-demographics and treatments
ECA study
Selected neighbourhoods in 5 US communities
1980-5
Each site - 3000 community residents and 500 residents in institutions were sampled (20,000 total)
2 interviews over a year using the DIS
DIS diagnosis of schizophrenia not congruent with psych classifications
ECA study - lifetime prevalences
Any disorder 32.3% Substance misuse disorder 16.4 Anxiety disorder 14.6 Affective disorder 8.3 Schizophrenia and schizophreniform 1.5 Somatization disorder 0.1
ECA study - anxiety disorder prevalence (1 month)
Phobia 12.5% Generalised anxiety and depression 8.5 OCD 2.5 Panic 1.6 Anxiety disorder were twice as common in women as they were in men
National Psychiatric morbidity survey 2000
1993-4
Conducted by OPCS (Office for Population Census and Surveys) using CIS (clinical Interview Schedule)
16-64 living in UK
10,000 interviews
Repeated in 2000 and upper age limit increased to 74
National Psychiatric Morbidity Survey - Findings
1 in 6 people in Britain have a neurotic disorder
• The most common neurotic/anxiety disorder was mixed anxiety and depression (88 cases per 1000), generalised anxiety was the next most common (44 cases per 1000)
• 5 per 1000 have a psychotic disorder
• Older people report less neurotic symptoms
• Prevalence rates were higher in women than men for all neurotics disorders except
panic (equal)
National Psychiatric Morbidity Survey - Findings (2)
44 per 1000 were classed as having a personality disorder, the prevalence being
slightly higher in men
• The most common personality disorder was anankastic (obsessive compulsive
personality disorder) (twice as common as all the others)
• The prevalence of alcohol dependence in the overall population was 74 per 1000
• 10% of people reported using illicit drugs in the year prior to interview, cannabis was
the most commonly used
World Mental Health Survey Initiative
Surveys in 28 countries
5000 interviews per country
Sample size >154,000
Interviews face to face by lay interviewers (trained)
Use the WMH-CIDI
The US has the highest prevalence of any disorder
Anxiety d most common followed by mood disorder
Male:Female ratios
Reading disorder 3-4:1 ASD 4-5:1 Asperger's 5:1 Tourette's 2-5:1 ADHD children 2:1 ADHD adults 1.6:1 Major depression 1:2 BPAD1 1:1 Panic with agoraphobia 1:3 Panic without agoraphobia 1:2 GAD 1:2 OCS 1:1 Specific phobia 1:2 Conversion disorder 1:2-10 Anorexia 1:9 Bulimia 1:9 BOD 1:3
Bipolar disorder - epidemiology
lifetime prevalence 0.3-1.5%
6/12 month prevalence - same
mean age of onset - 17 (community), 21 (hospital studies)
Gender M=F
Comorbidity - substance misuse and anxiety disorder
Major depression - epidemiology
lifetime prevalence 4-30%
6/12 month prevalence - same
mean age of onset - 27
Gender M:F 1:2
Comorbidity - substance misuse and anxiety disorder
Most prevalent in 18-44 group
People born since 1945 in industrialised countries have higher lifetime risk and earlier age of onset
Higher rates in women become apparent at puberty
Higher rates in unemployed, divorced, lower socio-economic class, urban areas
Major Depression - genetics
Twin studies - risk in 1st degree relatives is about 3 fold
MZ concordance rate = 45%
DZ concordance rate = 20% Heritability = 37%
Polygenic inheritance
GWAS have yet to report any convincingly replicated loci in depression
Monamine theory of depression
suggests that allelic variation in genes coding for monoamine synthesis or metabolism or specific receptors may contribute to the risk of mood disorders
Serotonin transporter gene
a particular allele has been shown to increase the risk of a subsequent episode of major depression when exposed to childhood adversity (Caspi et al, 2003)
Sociotropy
A strong need for approval
a/w increased risk of depression after adverse life events
Neuroticism
Measured by EPQ
Predisposes to major depression
Parental deprivation and depression
Death of parent in childhood - does not increase risk
Parental separation - increases risk, particularly divorce - due to discord and diminished care
Relationship with parents and depression
Physical and seual abuse clear risk factors
Non-caring and overprotective parenting styles are a risk (non-melancholic depression)
Depression - precipitating factors
Recent life events - 6 fold excess of adverse life events in months before onset
Poor social support
Physical illness - source of stress but can also have organic mood disorder e.g. HIV, endocrine, brain disease
Psychoanalytic theories - Freud
Mourning and melancholia
Loss of an ‘object’
Psychoanalytic theories - Melanie Klein
Weaning represents a major symbolic loss for the infant
Leads to attempt at reparation and concern for others
Failure in this can result in depressive reactions in the face of future losses
Psychoanalytic theories - John Bowlby
Insecure attachment can increase the risk of depression
Cognitive theories - Beck
Cognitive distortions such as arbitrary inference, selective abstraction, overgeneralization and personalisation lead to persistence of negative automatic thoughts.
Believes that dysfunctional beliefs (schemas) precede and predispose to depression.
The monoamine hypothesis
depressive disorder is due to abnormality in a monoamine neurotransmitter at one or more brain sites
noradrenaline and dopamine are catecholamines
5-HT function
Plasma tryptophan levels are decreased in untreated depressed patients
Shown in CSF studies (impulsive suicide attempts), neuroendocrine tests (blunted 5-HT neuroendocrine responses), imaging studies (decreased brain 5-HT1a receptor binding (PET) and decreased brain 5-HT re-uptake sites (SPECT and PET))
Noradrenaline function
Increased brain noradrenaline elevates growth hormone. GH response is blunted in depressed patients
Catecholamine synthesis can be reduced with AMPT. AMPT leads to depressive relapse in those with a personal h/o depression
Dopamine function
CSF levels of HVA are consistently low in depressed patients
AMPT leads to clinical relapse
Amino acid neurotransmitters
Decreased levels of glutamate in the anterior brain regions in depressed patients
Endocrine abnormalities
50% of patients with Cushing’s syndrome suffer from major depression
Addison’s disease, hypothyroidism and hyperparathyroidism also associated
HPA axis
Plasma cortisol secretion is increased throughout the 24h cycle in 50% of those with mod-sev depression
A/w enlargement of the adrenal gland
Increased cortisol response to ACTH challenge
Thyroid function
levels of free T3 may be decreased
1/4 of depressed patients have a blunted TSH response to TRH (also in alcoholism and panic disorder)
Organic causes of depression
Medications
Riserpine Interferon alpha Beta blockers Levodopa Digoxin Anabolic steroids H2 blockers Oral Contraceptives
Organic causes of depression
Drug abuse
Alcohol
Amphetamine
Cocaine
Hypnotics
Organic causes of depression
Metabolic
Hyperthyroidism Hypothyroidism Cushings Addisons Hypercalaemia (can be caused by Li or thiazide diuretics) Hyponatraemia DM
Organic causes of depression
Nutritional
Pellagra
Vit B12 def
Organic causes of depression
Neurological
Stroke MS Brain tumour PD Huntington's Epilepsy Syphilis Subdural haematoma
Organic causes of depression
Haematological
Anaemia
Leukaemia
Organic causes of depression
Other
Infection
Carcinoma
Revealed depression
Depressive symptoms present during acute psychotic episode but only become apparent as the positive symptoms resolve.
Post-schizophrenic depression
Has met criteria for schizophrenia in last 12m
Some schizophrenic sx still present but not dominating
Depressive sx fulfill the criteria for a depressive episode and present for at least 2 weeks
Depression - clinical features
Core features
Low mood
anhedonia
anergia
lack of interest
Depression - clinical features
Negative cognitions
Worthlessness
Hopelessness
Helplessness
Guilt
Depression - clinical features
Biological symptoms
Diminished sleep/insomnia Reduced appetite/weight loss Diurnal mood variation Psychomotor agitation/retardation Fatigue Reduced libido Constipation Anhedonia
Depression - clinical features
Other features
Suicidal ideation Poor concentration Self-neglect Isolative behaviour Anxiety/obsessional sx Somatic complaints Irritability Depressive stupor
Atypical depression
Klein and Davis’ description 1969
Low mood with mood reactivity and reversal of features normally seen in depression
Hypersomnia, hyperphagia, weight gain and libidinal increases
Tend to respond best to MAOIs
Response to TCAs is poor, SSRIs in the middle
Not in ICD-10
Psychotic depression
Psychotic symptoms indicate severe depression and usually mood congruent around themes of worthlessness, guilt
Persecutory delusions also seen
Cotard delusion
Delusional belief that they are already dead, do not exist, are putrefying or have lost their blood or internal organs
Dysthymia
Low-grade depressive symptoms for at least 2 years (1 year in adolescence)
Often early onset
Lifetime prevelance 3.6% (3-6%) (US)
Dysthymia (DSM criteria)
depressed mood for most of the day, for more days than not, as well as at least two of the following diagnostic symptoms: • poor appetite or overeating • insomnia or hypersomnia • low energy or fatigue • low self esteem • poor concentration or difficulty making decisions - hopelessness - normal mood for no more than 2 months - no episodes of major depression
Postnatal depression
Risk is 10%
Increased to 25% if there is a hx of depression
Increased to 50% if there is a hx of postpartum depression
Mod-sev depression = 3-5%
Risk is not influenced by obstetric factors (e.g. length of labour) or social class
Depression - treatment
First line - SSRI
Antidepressants are not 1st line for mild depression
Continue for at least 6 months after remission
If antidepressants are stopped immediately then 50% of patients experience a relapse within 3-6 months.
Continue for at least 2 years in pts with 2 prior episodes of depression
4 step approach
Depression - antidepressants
First SSRI Then another SSRI or newer gen hen venlafaxine, TCA or MAOI Augment with: Lithium, antipsychotics or another antidepressant (mirtazapine)
Refractory depression
Definition and treatment
2 successive failed attempts at treatment despite good compliance and adequate doses
Add lithium ECT Add T3 Combined fluoxetine and olanzapine Add quetiapine to SSRI or SNRI Add risperidone Add aripiprazole Bupropion and SSRI SSRI and venlafaxine, mirtazapine, or mianserin
Combining antidepressants
Irreversible MAOIs such as phenelzine and tranylcypromine are dangerous in combination with SSRIs - risk of serotonin syndrome
St John’s Wort
Effective in mild-mod depression but not recommended due to uncertainty about appropriate doses, variation in nature of preparations and potential serious reactions with other drugs
Can cause serotonin syndrome
Inducer of P450 system - decreases warfarin and ciclosporin, may also effect OCP
STAR*D Study
4 levels of treatment
Level 1 - citalopram for 14 weeks
Level 2 - swap to sertraline, bupropion or venlafaxine or augment with bupropion or buspirone. +/- cognitive psychotherapy
Level 3 - swap to mirtazapine or nortriptyline or adding on lithium or T3
Level 4 - swap to MAOI or ven + mirt
Outcome = remission
STAR*D Study - outcomes
Level 1 - 1/3 achieved remission, +10-15% responded
If levels 1 fails - 1 in 4 responded to switch, 1 in 3 responded to combination
50-85% who have a single episode will go on to have a second and 80-90% will have a third
Factors known to increase the risk of recurrence of depression
Family hx of depression • Recurrent dysthymia • Concurrent non-affective psychiatric illness • Female gender • Long episode duration • Chronic medical illness • Lack of a confiding relationship
Bipolar disorder - prevalence
Bipolar 1 - 1%
Bipolar 2 - 0.4%
Lifetime risk 0.3-1.5%
Peak age of onset 15-19 yrs
Usually begins as depression, 1st manic episode 5yr later
Average length of manic episode is 6 months
Drugs that precipitate mania
Levodopa
Corticosteroids
Anabolic-androgenic steroids
Antidepressants (TCA and MAOi)
Weaker evidence for: Dopaminergic anti-parkinsonian drugs, thyroxine, iproniazid and isoniazid, chloroquine
Gerald Klerman subtypes of bipolar disorder
1981
Bipolar III - cyclothymic disorder
Bipolar IV: Hypomania or mania precipitated by antidepressant drugs
Bipolar V: Depressed patient with a family history of bipolar illness
Bipolar VI: Mania without depression (unipolar mania)
Bipolar depression is different from unipolar…
Episodes are more rapid in onset
Episodes are more frequent
Episodes are shorter
Likely to involve reverse neurovegetative sx such as hyperphagia and hypersomnia
Features suggestive of mania rather than hypomania
Duration Flight of ideas Psychotic sx Loss of social inhibitions DSM - hypomania occurs without any marked social or occupational interference
Rapid cycling BPAD
10-20% of all patients with bipolar disorder
Tends to develop late in the course of the disorder and lasts less than 2 years in 50% of pts
Increased suicide risk
More common in women, earlier age at onset, greater illness burden, higher treatment resistance
More related to external factors such as life events, alcohol abuse, antidepressants and medical disorders rather than genetics
Medical disorders associated with rapid cycling
hypothyroidism Grave's disease SAH Stroke MS Head injury Drugs (propranolol, levodopa, cyproheptadine)
BPAD depression - treatment - NICE
No drug treatment - fluox + olanz or quet. If no response consider lamotrigine on own
On lithium - check level etc. Add fluoxetine with olanz or quet, or lamotrigine if no resp
On valproate: Increase dose to max then add fluox + olanz or quet. If no resp consider lamotrigine.
BPAD depression - treatment - Maudsley
1st choice - quetiapine
2nd choice - lithium or valproate
3rd choice - lamotrigine
3th choice - antidepressant plus mood stabiliser or antipsychotic
BPAD Mania/hypomania - treatment
Stop antidepressant
Antipsychotic - haloperidol, olanzapine, quetiapine or risperidone
Check Li levels if taking
If antipsychotic ineffective try another, if still ineffective add lithium, if this is ineffective or unsuitable consider valproate.
Do not offer lamotrigine
Children and young people 13+ - aripiprazole
Short term benzos
Acceptability of antimanic medication
Cipriani 2011
Best overall were olanzapine, risperidone, quetiapine and quetiapine
Rapid cycling - treatment
Combine lithium and valproate as first line
Second line: lithium monotherapy
Stop antidepressants
Evaluate precipitants
Consider combining mood stabilisers. Quetiapine best choice based on limited evidence
BPAD - long-term management
Lithium as first line, long term
If lithium is ineffective, consider adding valproate
If lithium is poorly tolerated or not suitable, consider valproate or olanzapine instead, or if prev effective during episode, quetiapine
NICE recommend li, olanz, quet, valp
Sodium valproate - s/e
hepatic failure
pancreatitis
suicidal behaviour and ideation
thrombocytopenia
Carbamazepine s/e
marrow suppression
hyponatraemia and SIADH
skin reactions, inc TEN and SJS
suicidal behaviour and ideation
Lamotrigine s/e
skin reactions, TEN, SJS
suicidal behaviour and ideation
blood dyscrasias
Gabapentin s/e
DRESS/multiorgan hypersensitivity
anaphylaxis/angioedema
suicidal behaviour and ideation
Topiramate s/e
acute myopia and secondary angle closure glaucoma
oligohydrosis and hyperthermia
suicidal behaviour and ideation
kidney stones
Other uses of lithium
Aggressive and self mutilating behaviour
Steroid induced psychosis
To raise WCC in people using clozapine
Reduced completed suicide in patients with BPAD
Valproate - side effects
Tiredness Significant weight gain (affects 30-50%) Tremor (25%) Hair loss (5-10%) Teratogenic effects
BPAD Mortality
8% of men and 5% of women hospitalised for BPAD died by suicide
Life expectancy is reduced by 13 years in men and 9 years in women
Schizophrenia - prevalence
1.4-4.6%
Schizophrenia - incidence
0.16 per 1000
Schizophrenia - gender
1:1
Schizophrenia
Increased risk/prevalence with…
winter births (5-15% higher) urbanicity migration and ethnic minorities (AESOP) lower socio-economic class LD (3% vs 1%) Family history Obstetric complications (prenatal nutritional deprivation, prenatal brain injury, prenatal influenza) no difference with race
Selection drift hypothesis
This suggests that people with schizophrenia tend to drift towards the lower class due to their inability to compete for good jobs etc
Schizophrenia and family history
Gottesman (1982)
Lifetime risk of developing schizophrenia
Gen pop 1% First cousin 2 Uncle/aunt 2 Nephew/niece 4 Grandchildren 5 Parents 6 Half sibling 6 Full sibling 9 Children 13 Fraternal twins 17 Off of dual matings 46 Identical twins 48
Schizophrenia and cannabis use
Overall, cannabis use appears to confer a two-fold risk of later schizophrenia or
schizophreniform disorder
People are 4.5 times more likely to be schizophrenic at 26 if they were regular cannabis smokers at 15, compared to 1.65 times for those who did not report
regular use until age 18
Lifetime risk of developing psychosis increased by 40% (odds ratio = 1.41) if a person had ever used cannabis (Moore, 2007)
Age at onset of psychosis for cannabis users was 2.70 years younger than for nonusers (Large, 2011).
Schizophrenia - macroscopic pathological features
Ventricular enlargement
Reduced brain vol (up to 5%)
Reduced left planum temporale gray matter, and reversed planum temporale surface area asymmetry (L larger than R in R-handed person)
Schizophrenia - microscopic findings
Reduction of the size of the dorsolateral prefrontal cortex
Reduction of the size of the hippocampus
AESOP study
Incidence of all psychoses was found to be higher in African-Caribbean (x9) and Black African (x6) populations compared to white british group.
Schizophrenia - Positive sx
Hallucinations
Delusions
Thought disorder
Schizophrenia - negative sx
social withdrawal apathy lack of energy poverty of speech (alogia) flattening of affect anhedonia Amisulpride has the most evidence for treating negative sx
Psychogenic polydipsia
Fluid drinking that greatly surpasses physiological requirements
Results in hyponatraemia - vomiting, agitation, ataxia, seizures, coma
Manage by fluid restriction
PANSS
7 positive symptom items, 7 negative and 16 general psychopathology
Each item scored on 7 point severity scale
Schizophrenia subtypes (ICD-10)
Paranoid Hebephrenic (disorganised) Catatonic Undifferentiated (doesn't conform to any subtype) Post-schizophrenic depression Residual Simple (predominate;y neg sx w/o being preceded by overtly psychotic sx Other Unspecified
Bouffee delirante
Brief short lived psychosis that last less than 3 months
Schizophrenia subtypes (Crow)
Type 1 - positive symptoms - excess of dopamine D2 receptors - respond better to antipsychotics
Type 2 - negative sx - underlying/anatomical abnormality such as ventricular enlargement or cortical atrophy - respond poorly to tx, chronic course, poor outcome
Schizophrenia: DSM-5 vs ICD-10
ICD-10 - sx present for at least 1 month, DSM-V - 6 months with 1 mnth active sx
Less than 1m in ICD - acute and transient psychotic disorder and DSM - brief psychotic disorder. In DSM if between 1-6m then its schizophreniform disorder
DSM requires some impairment of social and occupational dysfunction - not in ICD
Early onset schizophrenia
Affects 1 in 1000 children EOS - 13-18yrs VEOS - before 13yrs Insidious onset More severe premorbid neurodevelopmental abnormalities More frequent terrifying visual hallucinations Constant inappropriate of blunted affect Higher rate of familial psychopathology Minor response to tx Poorer outcome
Antipsychotics in schizophrenia - minimum effective doses
Chlorpromazine 200mg Haloperidol 2mg Sulpride 400mg Amisulpride 400mg Aripiprazole 10mg Olanzapine 5mg Quetiapine 150mg Risperidone 2mg
Antipsychotics in schizophrenia - maximum doses
Clozapine 900mg Haloperidol 20mg Olanzapine 20mg Quetiapine 750mg Risperidone 16mg Aripiprazole 30mg Flupentixol depot 400mg/week Zuclopenthixol 600mg/week Haloperidol depot 300mg 4 weekly
Antipsychotic Adverse Effects
Hypertension (mostly clozapine)
Reduction of the seizure threshold (esp clozapine)(haloperidol, sulpride and trifluperazine are good choices)
Sexual dysfunction (in order: risperidone, haloperidol, olanzapine, quetiapine, aripiprazole)
Weight gain
Antipsychotic weight gain - mechanisms
5-HT2c antagonism
H1 antagonism
Hyperprolactinaemia
Increased serum leptin (leading to desensitisation)
Antipsychotic weight gain - high risk
Clozapine
Olanzapine
Antipsychotic weight gain - medium risk
Chlorpromazine Quetiapine Risperidone Paliperidone Zotepine
Antipsychotic weight gain - low risk
Amisulpride Asenapine Aripiprazole Haloperidol Sulpride Trifluoperazine Ziprasidone
Tardive dyskinesia
Typically affects the face (75%), also limbs (50%) and trunk (25%)
Increasing dose of antipsychotic tends to lessen problem temporarily
Anticholinergics tend to worsen the movements. Believed to be due to postsynaptic D2 receptor hypersensitivity in the nigrostriatal pathway.
Develops over months to years
Risk factors for TD
Advancing age Females- not consistent finding Ethnicity - higher in african americans ?higher in affective disorders First gen antipsychotics Mental retardation Substance abuse
TD - treatment
Withdraw antipsych and switch to atypical e.g. clozapine or quetiapine
Discontinue anticholinergic
Tetrabenzine ( only licensed tx in UK - has depressogenic effects)
Benzos
Vit E (slows deterioration)
Ginkgo biloba
Propranolol
Schizophrenia - physical health monitoring
FBC, U&E, LFT - baseline and yearly lipids - baseline, 3m then yearly weight - baseline, freq for 3m then yearly glucose - baseline, 4-6m then yearly ECG - baseline and after dose change BP - baseline and freq during titration prolactin - baseline, 6m then yearly CPK - baseline, then if NMS suspected TFT - yearly if on quetiapine
Depots
Suggested role in…
Zuclopenthixol decanoate (has slight advantage in terms of efficacy) - aggressive patients
Flupentixol - depressed patients
Haloperidol - prophylaxis of mania
Pipotiazine palmitate - when EPSEs are a problem
Chlorpromazine
1st drug used for psychosis
Photosensitivity reactions
Clozapine
Reduced suicidality 30% would respond by 6wks A further 20% by 3m Additional 10-20% by 6m 30% do not respond (Meltzer 1992) Need level of 350-450ng/ml before a pt is considered resistant
Clozapine resistance - augmentation
Sulpride or amisulpride Lamotrigine Aripiprazole Haloperidol Risperidone Avoid: Pimozide, olanzapine
Clozapine resistance - other options
- Allopurinol + antipsychotic
- Max dose amisulpride
- Max dose aripiprazole
- D-Alanine and D-Serine
- ECT
- High dose olanzapine (usually tried first, if failed then…
- Olanzapine with various combinations
Lithium increases WCC - mechanism
?Stimulation of GM-CSF
?Demargination
No left shift
Clozapine levels (reference range)
350-500ug/L
Catatonia complications
Dehydration
DVT
PE
Pneumonia
Catatonia - treatment
Benzos (1st line)
ECT
Antipsychotics best avoided during acute phase
CATIE
Compared older vx newer antipsychotic meds
Phase 1 compared old and new antipsych
1400 participants
1 of 4 atypicals (OLZ, QTP, RIS, ZIP) or typical (perphenazine)
OLZ slightly better than others but weight gain significant
EPSEs not seen more with older drug
CATIE - Phase 2
Guidance on what to try next
If ineffective - tried clozapine
If intolerable - tried ziprasidone
Clozapine was much more effective than other atypicals
NCEP criteria for metabolic syndrome
• Central obesity: waist circumference 102 cm or 40 inches (male), 88 cm or 36
inches(female)
• Dyslipidaemia: TG 1.7 mmol/L (150 mg/dl)
• Dyslipidaemia: HDL-C < 40 mg/dL (male), < 50 mg/dL (female)
• Blood pressure 130/85 mmHg
• Fasting plasma glucose 6.1 mmol/L (110 mg/dl)
CATIE study - metabolic syndrome
The prevalence of MS at baseline in the CATIE group was 40.9%. By gender this was 51.6% in females and 36% in males. Male patients were twice as likely to have MS than matched controls, and female patients were three times as likely compared to matched controls.
Antipsychotic non-compliance in psychotic patients
25-75% - of these, 90% are intentional Following d/c from hospital non-compliance is: 25% at ten days 50% at one year 75% at 2 years
DAI
Drug Attitude Inventory
Assess’ patient attitude to medication - to predict compliance
Other scales: ROMI, Beliefs about medication questionnaire, MARS
Schizophrenia - course and prognosis
Ram (1992) concluded that over a 2 year period, one-third of patients with schizophrenia showed a benign course, and two-thirds either relapsed or failed to recover.
2-3 fold increased risk of premature death
The risk of dying over the next year for people with schizophrenia is 2.6 times higher than for people without it. (SMR 2.6) - mainly due to CVD
SMR falls with age due to early peak of suicides and gradual rise of population mortality
Agoraphobia
Age at onset: 20s
Gender distribution: F>M
12m prevalence: 1.8%
Specific phobia
Age at onset: childhood
Gender distribution: F>M
12m prevalence: -
Social phobia
Age at onset: late teenage/early 20s
Gender distribution: F=M (more F in comm)
12m prevalence: 2.3%
OCD
Age at onset: 25-35 years
Gender distribution: F>M
12m prevalence: 0.7%
PTSD
Age at onset:
Gender distribution: F>M
12m prevalence: 1.1-2.9%
GAD - Epidemiology
Prevalence (12m) - 4.4%
Rates in women are twice as high as in men
A/w lower household income, unemployment, divorce and separation
GAD - Cognitive Theories
Looming cognitive style - increased attention to potentially threatening stimuli, overstimulation of environmental threat, enhances memory of threatening material
Lack of a sense of control of events and of personal effectiveness
GAD - Personality
Personality traits - neuroticism
Personality disorder - anxious-avoidant
GAD - Neurobiology
- Amygdala and hippocampus implicated
- Noradrenergic neurons that originate in the locus coeruleus have been shown to increase arousal and anxiety
- GABA receptors are inhibitory and reduce anxiety, as fo the associated benzo-binding sites
- Probably a role for corticotropin-releasing hormone
GAD - Diagnosis
6 months with prominent tension, worry and feelings of apprehension about every day events and problems
At least 4 of following (and at least 1 of 1st 4)
(1) Palpitations or pounding heart, or accelerated heart rate
(2) Sweating
(3) Trembling or shaking
(4) Dry mouth (not due to medication or dehydration)
(5) Difficulty breathing
(6) Feeling of choking
(7) Chest pain or discomfort
(8) Nausea or abdominal distress
(9) Feeling dizzy, unsteady, faint or light-headed
(10) Feelings that objects are unreal (derealization), or that one’s self is distant or ‘not
really here’ (depersonalization)
(11) Fear of losing control, going crazy, or passing out
(12) Fear of dying
GAD - Diagnosis (2)
(13) Hot flushes or cold chills
(14) Numbness or tingling sensations
(15) Muscle tension or aches and pains
(16) Restlessness and inability to relax
(17) Feeling keyed up, or on edge, or of mental tension
(18) A sensation of a lump in the throat, or difficulty with swallowing
(19) Exaggerated response to minor surprises or being startled
(20) Difficulty in concentrating, or mind going blank, because of worrying or anxiety
(21) Persistent irritability
(22) Difficulty getting to sleep because of worrying
GAD Management - NICE
Step 1 - mild - education and active monitoring Step 2 - (no response to step 1) - low intensity psychological intervention Step 3 - (no response to step 2 or marked impairment) - high intensity psychological intervention or drug treatment Step 4 (no response to step 3 or marked impairment, comorbidity, risks) - complex drug/psychological treatment, input from MDT, crisis services, day hospital, inpatient care
GAD - Medication - NICE
Benzodiazepines should not be used beyond 2-4wks
1st line - SSRIs (sertraline) - warn of increased risk of suicidal thinking and self-harm if under 30 - weekly follow-up for 1m
If pt cannot tolerate SSRI or SNRI - offer pregabalin
Continue treatment for at least 1 year
Kava
Piper methysticum
Effective in reducing anxiety but a/w hepatotoxicity - not recommended
Specific phobia - epidemiology
Lifetime prevalence: men 7%, women 17%
Age of onset usually childhood
7 years for animals, 8 years for blood
Early twenties for most situational phobias
Specific phobia - Blood-infection-injury type
Bradycardia and hypotension often follow the initial tachycardia that is common to all phobias
Genetic link - may have particularly strong vasovagal reflex
Specific phobia - treatment
Behaviour therapy
Graded exposure