Psychotic Disorders

Psychosis = a mental disorder causing an inability to distinguish between reality and
imagination, characterised by delusions and hallucinations.



 Brief psychotic episode
 Schizophreniform disorder
Schizoaffective disorder
Delusional disorder
Post-partum psychosis
Psychotic disorder NOS (Atypical psychosis)

i. Schizophrenia
A psychotic disorder or unknown aetiology and variable presentation, characterised
by positive and negative (deficit) sx’s. Although not a cognitive disorder, the condition
often causes cognitive impairments.
 1% of population (no gender difference)
 Most common in people aged 15-35yrs; Rare in people aged <10yrs or >40yrs
 Average onset younger for men than women (18-25yrs vs. 25-35yrs)
Causative or Contributory Factors
Genetics & Family Hx:
 Adoptive MZ studies show ~50% concordance rate vs. 12% in DZ twins
 Greater genetic loading = Greater risk (40% in child of two parents with
schizophrenia, 12% in child with one schizophrenic parent)
 8% in non-twin sibling of patient with schizophrenia
○ 10% of a patient’s 1st degree relatives are likely to be schizophrenia sufferers
Birth Cx’s: Schizophrenia is specifically associated with birth trauma and foetal
hypoxia, but contribution is small (~5%)
Infection & Birth Season: children born in winter have a higher risk of
schizophrenia (5%). A viral cause is the suspected link.
Psychosocial Stress: first episode (precipitant) or relapse is commonly
correlated with stressful life events eg. Marriage breakdown
Low socioeconomic Class: This class has a disproportionate number of
patients. Whether this is a cause or effective of the illness is uncertain.
Dopamine hypothesis
Hyperactivity of the dopaminergic system (dopamine release, number /
hypersensitivity of receptors) is supported by:
 Efficacy of dopamine D2 receptor antagonists (typical antipsychotics) in Rx
 Drugs that dopaminergic activity induce psychosis eg. Amphetamines
Serotonin (5-Hydroxytriptamine)

Increasing research into the role of 5-HT given efficacy of dopamine-serotonin
antagonists (SDA’s – atypical antipsychotics) in Rx. Further, Lysergic acid
diethylamide (LSD) affects 5-HT levels and causes hallucinations.
Limbic System
System including many cortical and sub-cortical structures, it’s role is controlling
emotion, motivation, and emotion associated with memory.
Decreased size in patients with schizophrenia shown by MRI
Ventricles & Cortex
MRI and CT have consistently shown increased lateral, third and cerebral
ventricular size and reduced cortical volume. However, ventricular size are
usually still within normal limits.
DSM IV-TR Diagnostic Criteria


Nb. Only 1 Sx required if
A. ≥2 Characteristic (cardinal) Sx’s:
delusions are bizarre, or if
1. Delusions
hallucinations consist of a
 Paranoid or persecutory delusions
running commentary or two
 Delusions of grandeur
or more voices conversing
 Delusions of reference eg. TV talking about them
with each other.
 Somatic delusions eg. of terrible illness
2. Hallucinations
3. Disorganised speech / thought (eg. frequent derailment or incoherence) aka
“word salad”
4. Grossly disorganised or catatonic behaviour
 Variously characterized by stupor/inactivity, mania, odd posturing for an
extended time, catatonia, rigidity or extreme (waxy)flexibility of the limbs
5. Negative Sx’s:
– Flat or blunt affect
– Marked apathy & Lack of motivation
– Poverty of speech & speech content
– Blocking of thought
– Poor grooming
– Social withdrawal
B. Social / Occupational Dysfunction for a significant portion of time since the
onset of sx’s
C. Duration: Continuous signs / sx’s persist for ≥ 6 months
D. Schizoaffective and Mood disorders excluded
E. Substance / General medical conditions excluded

Positive Sx’s: Reflect an excess or distortion of normal functioning eg.
hallucinations, word salad
Negative Sx’s: Reflect a loss of normal functioning eg. dishevelled
appearance, withdrawal

Clinical Features
No single feature is pathognomonic for schizophrenia.
Schneiderian 1st Rank Sx’s
 3 types of auditory hallucinations
– Third person
– Running commentary about the pt
– Thought echo
 3 types of thought disorder
– Thought insertion
– Thought withdrawal
– Thought broadcasting (‘read’ by others)
 Passivity
– Made Feelings & Actions: An external agency controls their feelings
– Somatic passivity: Similar to made feelings, pt feels that they are a
passive recipient of bodily sensations from an external agency
 Delusional perception
– A real perception (such as a real objective sound) which is followed by
misinterpretation of that perception
In the absence of organic cerebral pathology, the presence of any of the above is indicative
of schizophrenia.

Pre-morbid sx’s may include having few friends at school / college, being socially
withdrawn, acute onset of OCD. Often their pre-morbid personalities are quiet,
passive and introverted.
Sub-types: 4 Major DSM Types
1. Paranoid:
▪ Characterised by the presence of delusions & auditory hallucinations, typically
▪ Does not have any other positive sx’s (incoherence, loosening of
associations, flat or inappropriate affect, catatonic behaviour, etc)
▪ Sub-type with later onset and the best Px
2. Disorganised (hebephrenic):

Characterised by marked regression to primitive, uninhibited and
disorganised behaviour.
Marked positive & negative sx’s; Inappropriate bursts of laughter and
cognitive & attention deficits
Subtype is usually early onset and a/w poor Px.

3. Catatonic:

Classic feature is marked disturbance in motor function eg. Stupor, rigidity,
excitement, posturing
Marked negative sx’s. Also a/w poor Px.

4. Undifferentiated:

Marked positive sx’s but does not meet the criteria for any other type

Sub-types: Type I vs. Type II

This system of classification is not accepted by the DSM, but clinically has been
significant with respect to research. It is based on whether the patient demonstrates
positive or negative sx’s.
 Type I patients have mostly positive (or productive) sx’s, including delusions and
hallucinations, acute onset, normal brain structures on CT, and relatively good
response to Rx, good Px.
 Type II patients have mostly negative sx’s, chronic onset, structural brain
abnormalities on CT, poor responses to Rx and poor Px.
General Appearance & Behaviour:
Appearance may range from dishevelled to obsessively groomed
Behaviour may be unprovoked agitation and violence to catatonic
Speech may be talkative or silent
Mood & Affect:
Affect may be flat, blunted, inappropriate, labile.
Stream – can be slow, normal or manic
Form – Formal thought disorder ie. derailment, tangentiality, blocking,
circumstantiality, loosening of associations commonly seen (also in mania),
Content – delusions characteristic
Perception: Auditory and visual hallucinations are common, but in the other
modalities it is unusual. Illusions may also occur in any phase of the illness.
Consciousness & Cognition: Consciousness may be depressed (in stupor) but
usually normal. Orientation and memory are usually normal. Attention / Cognition can
be affected. Classically, insight into their illness is poor, correlated with lack of
compliance. Judgement is poor with psychosis.
Rapport: often difficult to build rapport with patients, as agitation can occur without
i. Psychotic disorder due to a general medical condition
 Hyper- / Hypothyroidism
 Cushing’s disease or syndrome
 Chest infection
 Vitamin B12 or folate deficiency
 Meningitis
 Space-occupying lesions (may cause visual hallucinations)
 Must always pursue an undiagnosed non-psychiatric medical condition in
patients exhibiting unusual or rare sx’s or any variation in consciousness
ii. Medications / Substance Abuse
 Medications (levodopa, antipsychotics, steroids, tranquilizers)
 ETOH withdrawal, Lysergic acid diethylamide (LSD) usage, etc.
iii. Other psychotic disorders
 Brief psychotic disorder = schizophrenic sx’s lasting between 1 day and 1
 Schizophreniform disorder = schizophrenic sx’s lasting between 1 and 6
 Schizoaffective disorder = bipolar or depressive syndrome develops
concurrently with the major schizophrenic sx’s but where psychotic sx’s
persist despite remission of mood disorder sx’s.

A further deterioration of baseline functioning occurs after each relapse of psychosis. Seizure disorders  Mood disorders can be a feature of epilepsy post-seizure vi. This failure to return to baseline functioning is the key distinction between schizophrenia and the mood disorders. episodes of major mood disorders and suicide attempts. worthlessness.  Bipolar disorder: commonly delusions (grandiose) & manic behaviour during episodes of mania though hallucinations are rare  MDD and antipsychotics can also cause ‘negative’ symptoms v.4  ~50% can be described as having a poor outcome. 5-10% cocaine. A minority will only have one schizophrenic episode. tongue. Mood Disorders with Psychotic sx’s  MDD: delusions typically consistent with depressed mood (ie. Pericyazine. Acute dystonia. and 10-15% die by suicide. Anticholinergic SE’s (especially Thioridazine). Tardive dyskinesia. EP Sx’s (rigidity. if agitated) ○ Often cause significant SE’s: Akathisia (restlessness). Fluphenazine. Thioridazine // Haloperidol. Neuroleptic malignant syndrome ○ SE’s (first 3): Marked sedation (often exploited). Flupenthixol ○ Used as 2nd line Rx ○ Effective for Rx of the positive sx’s & for sedation (eg. sexual and work hx’s – Mood disorder sx’s (especially depressive disorders) – Positive sx’s – Good support systems Cx’s  Suicide: ~50% of patients will attempt suicide. lips & face  Often irreversible & rarely occurs until after 6months of Rx  Prevention is the only way to Rx this adverse effect . Malingering / Factitious disorders  Natural Hx Classic course of schizophrenia is exacerbations and remissions. etc. Fluphenazine. One third are markedly impaired and require frequent hospitalisations. tremor).  STDs: Patients are statistically more likely to practice more sexually risky behaviours (10 times increased risk of HIV)  Increased all-cause morbidity: ~double the requirement of physical healthcare  Increased all-cause mortality: 3-fold relative to normal population Pharmacological Therapy Dopamine receptor antagonists [Typical antipsychotics] Chlorpromazine. exacerbation of sx’s. One third have continual sx’s but can function within society.2 Factors associated with a good prognosis include: – Late and / or acute onset – Obvious precipitating factors – Good premorbid social. Flupenthixol Tardive dyskinesia  Involuntary choreiform movements/tics of mouth. with repeated hospitalisation.Delusional disorder = non-bizarre delusions present for ≥ 1 month w/o other schizophrenic sx’s iv. Prognosis  Rule of thirds: One third have somewhat normal lives. mood congruent delusions) such as guilt. Sun sensitivity & sunburn (Chlorpromazine).  Depression: Lifetime risk of MDD is 50% and it contributes to risk of relapse (despite sx’s of mood disorders being a good prognostic factor)  Drug & ETOH abuse: 30-50% ETOH. 15-25% cannabis. ○ Depots: Haloperidol.

Olanzapine (Zyprexa). Quetiapine (Seroquel). Safety Assessment Risk of patient to themselves (risk of repeated attempts + risk of successful suicide) & to others must be assessed (Low.Serotonin-Dopamine Antagonists (SDAs) [Atypical antipsychotics] Risperidone (Risperidal). Medium. lithium. Aripiprazole (Abilify). Long-term Rx Pharmaceutical:  SDA’s (atypical) should be mainstay. High) 2. carbamazepine. Clozapine (Clozaril)  Used as 1st line Rx for schizophrenia & psychosis  Antagonises different dopamine receptors as well as 5-HT receptors  Much more effective for –ve sx’s and at least as effective for +ve sx’s  Minimal or no extrapyramidal sx’s (except risperidone) due to looser bonding at D2-receptor sites  Depots: Risperidal consta CNS: Extrapyramidal Sx’s (EPS) Tardive dyskinesia Sedation Seizures Other: Neuroleptic malignant Syn. Weight gain Orthostatic Hypotension Anticholinergic SE’s Prolactin Liver transaminases Agranulocytosis Typical Agents Risperidone Olanzapine Quetiapine Clozapine +++ 0 to ++ 0 to + 0 0 +++ + 0 0 0 + to +++ 0 to + + 0 + + +++ 0 +++ +++ + + + ? + 0 to ++ + +++ + +++ + to +++ + + 0 ++ 0 to +++ 0 + 0 +++ +++ + to ++ 0 0 0 0 to ++ 0 to + +++ (2%) 0 to + 0 to + 0 0 0 0 +++ (1%) (Kaplan & Sadock. long-term use of DA’s (typical) is highly questionable due to risk of tardive dyskinesia  > 1 antipsychotic at a time is rarely (if ever) indicated  Minimum length of antipsychotic trial is 4-6 weeks  Use lowest effective dose but monitor plasma levels [Clozapine requires monthly FBE’s to monitor agranulocytosis]  Combination with other drugs (eg. 4. Screen for medical causes of psychosis) 3. Ix of causes & Dx (eg. 2001) Mx 1. BZD’s) may be indicated for resistant or complicated cases . Immediate Rx Antipsychotics (except clozapine) are remarkably safe and can be given in ER situations w/o conducting physical or lab examinations.

3rd edn. 6. Benztropine (Cogentin) Electroconvulsant Therapy (ECT)  Efficacy << Antipsychotics. FIRSTConsult. < http://en. 2003) References 1. ‘The limbic system’. ‘Schizophrenia’.net.firstconsult. Kaplan & Sadock (2001). Blackwell publishing. 3rd edn. Sadock & Sadock (2004). 5.wikipedia.hcn. but efficacy depends on emotional temperature (‘expressed emotion’). Non-responsiveness: Lack of clinical improvement despite the use of at least 2 antipsychotic drugs prescribed for reasonable durations (4-6wks) 2. Katona C & Robertson M (2005). Wikipedia. Cognitive behavioural and Individual have less evidence for efficacy. ▪ Case Management: Coordinates parties supporting the patient. Intolerance: The inability to achieve adequate benefit with other antipsychotics because of severe and untreatable neurological SE’s (EP SE’s or tardive dyskinesia) Contraindications:  Previous hypersensitivity to clozapine  Hx of granulocytopenia / agranulocytosis (from clozapine or otherwise)  BM disorders or BM suppressive drugs  Circulatory collapse and / or CNS depression due to any cause. Clozapine Indications: 1. myocarditis)  Severe hepatic disease including active liver disease  Uncontrolled epilepsy  Paralytic ileus (MIMS online. benztropine) Typical antipsychotics (and Risperidone) may be given together with anticholinergic agents to prevent EPS sx’s eg. Psychiatry at a glance. pp. 2003 < http://mims. Pocket handbook of clinical psychiatry. those with catatonia. < http://www. MIMS online. Lippincott Williams & Wilkins. benzhexol.g. Australia.  Alcoholic and other toxic states  Severe renal or cardiac disease (e. efficacy largely dependant on the individual case manager. but may be indicated for those non-responsive to antipsychotics. ▪ Other therapy such as > 4. Concise Textbook of Clinical Psychiatry. 134-153 3. Rx Extrapyramidal sx’s and Acute dystonia with anticholinergics (eg. or those with severe depressive sx’s Psycho(social) Therapy ▪ Social / Behavioural skills training: shown to relapse rates as measured by the need for hospitalisations ▪ Family Therapy: most effective psycho-therapy in terms of sx’s & > 2. Also educated family & patient about condition and how to best > .

poverty of ideas) Delusions. poor grooming. birth. Medical: eg. blunted. labile. most commonly Auditory Thought Stream Form Content Cognition Consciousness Attention & Concentration Executive function Orientation & Memory Judgement & Insight Frontal lobe can be affected. Selfesteem. bizarre or colourful clothing. entertaining S: Pressured. unemployment. tangentiality. Poor memory. expansive. NA. dramatic. Cortical volume. causing cognitive deficits. obsessive rumination. Delusions possible. MZ:DZ  60:20. A: Labile & swinging Hallucinations less common Normal Derailment. Agitated. neologisms. Cushing’s Behaviour: Variable (eg. worthlessness. NA & DA levels Psychosocial stressors Genetics: 25% with one parent. ♂ = ♀ Genetics ( with FamHx. loosening of associations Slowed 10% have sx’s of Thought disorder (blocking. S: Slowed. long pauses. Thyroid Bipolar (Manic) Mood disorder ~1% population. M: Depressed.Disorder type Epidemiology Aetiology MSE Appearance. intrusive. guilt. incoherent M: Euphoric. MZ>DZ concordance but still less than Bipolar. passivity. sad A: Constricted or labile Hallucinations rare A: -motor agitation. irritable. MZ:DZ = 50%:10%) Dopamine (& 5-HT) hypothesis Psychosocial stress Ventricle size. clang-assoc. hallucinations rarer. tangentiality. monosyllabic. non-spontaneous. Normal Impaired Normal Extremely impaired judgement and insight is the hallmark of mania . ♂:♀ = 1:2 5-HT. excess makeup B: Hyper-excited. irritable. Grandiosity. postured. circumstantiality. Genetics: Less important than for Bipolar I. ideas of reference. Medical: eg. ♂ = ♀ 5-HT. soft. circumstantiality. poor eye contact. inappropriate Perception Hallucinations. withdrawn. DA Psychosocial: loss of parent or spouse. loud. Suicidal ideation (60%) Negativity is customary. Behaviour & Speech Schizophrenia Psychotic. Impaired judgement Insight: Sx’s often overemphasised Normal Mood & Affect A: Flat. Normal (Unless catatonic) Normal Decreased Increased (excitable) Distractible. flirtatious. poverty. 50-75% with two. Fast (‘racing thoughts’) Flight of ideas (severe can be incoherent). Difficulty concentrating Impaired abstract thought Easily distracted Orientated. +ve & -ve sx’s 1% population. mood congruent delusions. monotone. catatonic) Speech: Normal to incoherent A: -motor retardation agitation. tearful. and Amygdala & hippocampus size Depression Mood disorder 20% popn. threatening. frustrated.

Setraline (SSRI) Dopamine (DA)  Drugs that reduce DA and diseases that reduce DA concentrations (eg. but +ve results also occur in other psychiatric illnesses Thyroid . which are themselves indivisible. child has 50-75% chance.  Data suggests that dopamine activity is associated with depression and activity with mania. Genetic: Genetic factors are much more significant in Bipolar I disorder than MDD. st  1 degree relatives of someone with MDD have a 10% chance Adoption Studies:  Biological children of affected parents remain at risk even if reared in nonaffected adoptive families. usually with a return to normal functioning in b/w episodes. Aetiology of Mood Disorders: Some clinicians believe stress is the primary cause of depression. drugs that DA concentrations (eg. Medical / Hormonal factors: Cortisol (Cushing’s Syn. In contrast. Twin Studies:  Concordance rate for MDD in monozygotic twins is ~50%  Concordance rate for bipolar I in monozygotic twins is between 33-90% Neurobiology: Serotonin (5-HT)  Efficacy of Selective Serotonin Re-uptake Inhibitors (SSRI’s)  Depletion of serotonin may precipitate depression Noradrenaline (NA)  Down regulation of β-Adrenergic receptors is associated with depression  Efficacy of clinical anti-depressants which also block NA-receptors eg. if both have Bipolar I.Mood Disorders Psychopathological conditions in which a persuasive disturbance of mood is the primary feature. child has 25% chance of a mood disorder. amphetamines) reduce the sx’s of depression. Family Studies: st  1 degree relatives of Bipolar I disorder have 8-18 times risk of Bipolar I and 2-10 times risk of MDD  If one parent has a Bipolar I. Parkinson’s) are associated with depressive Sx’s. but no specific gene has yet been identified. Tricyclic anti-depressants. but depressive illnesses involve both mind and body. whilst others believe its role is limited. / disease) ○ Correlation with cortisol and depression has been one of the oldest observations in psychiatry. Aetiology is really a mix of genetic and environmental factors. non-suppression of cortisol) may correlate with relapse rates. ~50% of depressed patients have cortisol levels ○ New data suggests that a +ve Dexamethasone-Suppression Test (DST) (ie.

Clinical depression. . 5-12% men (♀:♂ = 2:1)  Mean age of onset ~40yrs (50% cases between 20-50yrs). Concentration and decisiveness viii. Multiple sclerosis and cancer carry an especially increased risk ○ L-Dopa & Interferon are medications known to precipitate depression Psychosocial Factors: Life Events & Environment ▪ Stressful life events more often precede the first (rather than subsequent) episodes of mood disorders ▪ The life event most often a/w depression is losing a parent < Age 11 ▪ Environmental stressor most often a/w depression is loss of a spouse ▪ Unemployed have 3 times risk of depression compared to employed ▪ Childbirth: 45% of women who develop bipolar have their first episode in the post-partum period Cx’s  Suicide and self-harm – 10-15% of depressed pt’s will commit suicide. Major depression. i. Fatigue vi. helplessness or guilt Major Depressive Disorder (MDD) is the Dx with ≥ 2 depressive episodes. Cases <20yrs increasing  Highest risk category = Women aged 25-44  No correlation with socioeconomic status Lifetime prevalence is the proportion of people who will suffer the illness at some stage in their lives DSM IV-TR Dx Criteria Major depressive episode: Dx by the DSM-IV-TR requires the presence of 5 (or more) of the following sx’s that last essentially without remission for ≥ 2 weeks. Depressed mood for most of each day ii.○ Thyroid disorders found in 5-10% of depressed patients Physical Illness & Medications ○ The major cause of depression in later life ○ HIV. Epidemiology:  Lifetime prevalence is 10-25% women. Insomnia or Hypersomnia vii. 66% will have suicidal ideation  Risk of CVS event Major Depressive Disorder (MDD) Synonyms: Unipolar depression. Significant Weight or Appetite v. Psychomotor agitation or irritability ix. Feelings of worthlessness. Anhedonia = Loss of interest/pleasure in normally pleasurable activities Either of these 2 must be one of the 5 sx’s iii. Recurrent thoughts of death or suicide (MUST ASK!) iv.

 Mania: 5-10% with MDD have a manic episode within 10yrs of their Dx. Prognosis (MDD)  MDD is not a benign condition – it tends to be chronic and pt’s tend to relapse  Post-hospitalisation 25% relapse within 6mths  10-15% will commit suicide. the risk of dying in the event of OD is increased. Fluvoxamine (Movox). Minor depressive disorder: Incomplete but episodic depressive syndrome Recurrent brief depressive disorder: Complete depressive disorder lasting < 2 weeks duration Associated Disorders  Anxiety: Anxiety is a common sx of depression (up to 90%). even at high doses (eg. Paroxetine (Aropax).& βadrenergic. Hyponatremia. rates of self-harm are higher 1St Line Pharm. Incomplete depressive syndrome without episodes of normal functioning. In addition.Dysthymic disorder: Chronically depressed mood (for ≥ 2 years) but without enough sx’s to fulfil the DSM criteria for MDD ie. each one can have very different characteristics and efficacy between pt’s Eg. Fluoxetine (Prozac). Selective Serotonin Re-uptake Inhibitors (SSRI’s) Citalopram (Cipramil). Fluoxetine has a very long ½ life  SSRI’s have a relative lack of SE’s. Untreated episodes last 6-13months  Withdrawal of antidepressants < 3mths almost always results in return of sx’s  Over a 20yr period. initial anxiety may occur (suicide risk) so must Rx with BZD’s. OD)  SE: Sexual dysfunction (commonest complaint). Sleepiness. low affinity for . Setraline (Zoloft)  Selectively inhibits CNS neuronal reuptake of serotonin. ▪ Specific antidepressant-free intervals must be observed when changing between antidepressants ▪ Combinations of antidepressants have not been shown to be more effective than monotherapy and there is a very significant risk of serious SE’s. efficacy with matching toxicity  Potent inhibitor of CNS neuronal 5HT and NA reuptake  Only antidepressant to cause hypertension (most cause hypotension) Reversible Monoamine Oxidase Inhibitor (MAOI) Moclobemide (Arima) . DSM IV has criteria for the existence of mixed anxiety-depressive disorder  Drug & ETOH abuse / dependence (eg. trials should last at least 3 weeks. withdrawal reaction if stopped suddenly (as with all CNS drugs) Serotonin-Noradrenaline Reuptake Inhibitor (SNRI) Venlafaxine (Efexor)  Like a ‘suped-up’ SSRI. dopaminergic and muscarinic receptors  Despite many SSRI’s. the mean number of episodes is 5-6. Rx (MDD) ▪ Antidepressants take ≥ 14days to have effect. cocaine or amphetamines used in MDD) Natural Hx (MDD)  Onset: ~50% have depressive sx’s before the first identified episode  Duration:  Treated episodes last ~3mths.

SE’s similar to SSRI’s otherwise .  Reversible inhibitor of monamine oxidase A (MAO-A) to CNS monoamines Only antidepressant that does not cause sexual dysfunction.

ataxia & tremor  Autonomic instability with possible rapid changes in vital signs  Myoclonus. postural hypotension 2nd Line Pharm. ○ SE’s: postural hypotension. Duration of action = 2-3 weeks while new enzymes form.and 5HT3-receptors. pate) and cold & flu medications may cause significant hypertension & CVA / CVS events Mianserin ○ Tetracyclic antidepressant. anorgasmia.Mirtazapine (Avanza)  Blocks 2-receptors causing release of 5HT & NA. Alpha-adrenergic SE’s (sedation. hyperthermia  Delirium. cheeses. Anticholinergic SE’s (dry mouth. CVS disease. constipation. Rx (MDD) Tricyclic Antidepressants (TCA’s) Amitriptyline. sedation. It is not recommended for Rx of severe depression. failure of ejaculation. Nortriptyline. urinary retention). constipation. the most serious of which is the Serotonin syndrome:  Diarrhoea & Restlessness / Extreme agitation  Hyperreflexia. blurring of vision. Works identically to mirtazapine but is a 2nd line agent St John’s Wart Systematic reviews found there was no significant difference between St John's wort (hypericin) and other antidepressants for Rx of mild-moderate depression. usually in the evening ○ SE: Use is 2nd line due to lethal cardiotoxicity in OD. weight gain). Paradoxically. Tranylcypromine ○ These non-selective monoamine oxidase inhibitors (MAOIs) irreversibly inhibit the enzymes MAO-A and MAO-B. coma and CVS collapse & death SSRI’s should not be co-administered with a MAOI. impotence. Imipramine. blurred vision. lithium or L-trytophan as 5HT levels may occur and cause this syndrome. results in [monoamine] in brain and other tissues. dry mouth. . Monoamine oxidase inhibitors (MAOIs) Phenelzine.  Have long elimination ½ lives. some patients experience sedation and fatigue. insomnia and arousal. allowing once daily dosing  SE: Notorious for weight gain. sexual dysfunction. enhancing 5HT1 serotonergic transmission. and also block 5HT2. ○ C/I: Various foodstuffs with high amine concentrations (eg. Switching Medications & ‘Serotonin Syndrome’ An appropriate interval should be observed between changing antidepressants to avoid adverse effects. Dothiepin ○ Non-selective reuptake inhibitors of 5HT & NA ○ Extensively metabolised in the liver ○ Long ½ lives allow once-daily admin. postural hypotension. home-brewed alcoholic beverages. ○ C/I: Suicide intent (OD risk). seizures. bladder neck obstruction. glaucoma.

with a return to normal functioning in between. Goal-directed activity or psychomotor agitation vii. Other psychiatric illnesses (eg. feels rested after only 3hrs sleep) iii. schizophrenia) have been excluded as cause of manic episode. 10-20% have manic episodes only. Bipolar II Disorder: Recurrent major depressive episodes with hypomanic syndromes ie.Bipolar Disorder Synonyms: Manic depression Bipolar disorder is a term to describe a recurrent illness characterised by episodes of either mania and / or depression. Inflated self-esteem or grandiosity ii. less severe & no psychosis) Bipolar I Disorder: Complete manic and depressive syndromes. sexual indiscretions. Distractibility vi. Other psychiatric illnesses (eg. 3 (or more) of the following sx’s persist to a significant degree during the mood disturbance: i. or there is risk of self harm. or the episode requires hospitalisation. Excessive pleasurable activities that have high potential for detrimental consequences (eg. where depression predominates. More talkative than usual or pressure to keep talking iv. Bulimia nervosa  Attention deficit hyperactivity disorder (ADHD) and / or conduct disorder. especially with juvenile onset (57-98%)  Borderline personality disorder Natural Hx (Bipolar) . foolish business ventures) C. buying sprees. schizophrenia) have been excluded as cause of hypomanic episode. Hypomanic Episode: All the same criteria as for a Manic episode BUT the episode is not severe enough to fulfil criteria C (ie. social phobia  Antisocial behaviours eg. 90% of cases are apparent by 30yrs age  Men have more manic episodes whilst women have more depressive episodes  Higher then average incidence in upper socioeconomic groups DSM IV-TR Dx Criteria Manic Episode: A. Flight of ideas / Subjective feeling that thoughts are racing v. or there are psychotic features. spouse abuse. Cyclothymic disorder: incomplete depressive and manic syndromes Associated Disorders (Bipolar):  Drug & ETOH abuse and dependence  Anxiety disorders eg. Abnormally and persistently elevated or irritable mood lasting ≥ 1 week B. Panic disorder. Gambling. child abuse  Eating disorders eg. Epidemiology:  ~1% prevalence (♀:♂ = 1:1)  Mean age of onset ~30yrs (may be as early as 5yrs old). Marked impairment in occupational or social functioning. Need for sleep (eg.

If Olanzapine is the primary Rx.  Additional antidepressant action in 1/3 of pt’s Olanzapine (Zyprexa): Atypical antipsychotic indicated in acute mania Lamotragine (Lamictal): a 1st line prophylactic agent. warfarin. both acute episodes and prophylaxis. OCP) but can be used in acute episodes and for prophylaxis. but as they may precipitate manic episodes and rapid cycling. they are: a) Never given in an acute manic episode b) Usually withdrawn after 1-2mths after successful resolution of bipolar depression Combination Rx  Patients who fail to respond to monotherapy in acute or prophylactic settings do benefit from combination therapy . Additional antidepressant action in 1/3 of pt’s.  Renal toxicity is the most important SE. Weak antidepressant properties. Iatrogenic properties (neural tube defects). weight gain. 45% have > 1 episode  Early onset is a/w poor prognosis Pharmacological Rx (Bipolar) Getting the correct Dx of Bipolar disorder is essential to Rx. both acute episodes and prophylaxis. Bipolar is not Rx with antidepressants alone as this will precipitate manic episodes and contribute to rapid cycling. Carbamazepine (Tegretol):  2nd line Rx as it is a potent enzyme inducer so many drug interactions (eg. and some nonresponsive to Li may respond to valproate  SE: hair loss. tremor and sedation. but 10-20% have only manic episodes Untreated manic episodes last ~3mths Prognosis (Bipolar)  Bipolar patients have a poorer prognosis than patients with MDD  40% have a chronic disorder. but not for acute episodes Adjunctive antipsychotics / BZD’s (Mania) Manic episodes may require the addition of an antipsychotic or BZD. but thyroid and dermatological effects can also occur  May be combined with mood stabilisers for refractory cases Sodium Valproate (Epilim):  Alternative to Li also considered 1st line Rx for mania. and the most common BZD used in diazepam (Valium). but it depends on the primary Rx eg. addition of another antipsychotic is not recommended. Mood Stabilisers (Mania) Lithium:  Considered 1st line Rx for mania. Atypical antipsychotics are used first (better SE profile). Antidepressants (Bipolar Depression): Choice of antidepressant is similar to that for MDD.   Most often starts with depression (~70% of cases) but is a recurring disorder Most patients experience both depressive and manic syndromes.  Many tolerate valproate better the Li and carbamazepine.

from laughter to irritability to depression in mins. pseudodementia). any depressive feelings Often emotionally labile. Insight is often very limited also. etc. Pt’s who threaten as they begin to improve as they regain important people (President of USA) have Bipolar I disorder rather than energy (paradoxical suicide). Rate & Volume Cannot be interrupted whilst speaking. pulling hair. ~10% have Stream is unrestrained & accelerated marked sx’s of thought disorder Form is disturbed (eg. ‘Mood incongruent’ delusions would include those of grandiosity. Volume and rate increase Single word responses Depressed mood. overemphasise their sx’s). Delusions congruent with a depressed Bizarre & mood incongruent delusions mood are said to be ‘mood congruent’. In combination with pharmacological Rx. (great wealth & power) typically.) Manic Episodes (Bipolar) Excited. Content includes themes ideas) of self-aggrandisement. but can be effective (and life saving) in refractory manic or depressive episodes  Safe in combination with Li  C/I: MAOIs. MSE General Appearance Speech Mood & Affect Thought Perception Sensorium & Cognition Judgement & Insight Impulsivity Depressive Episodes Psychomotor Retardation or Agitation (hand wringing. but they are not recommended as the only Rx for bipolar disorder. No obvious cognitive defects causing poor memory (depressive but patients are often easily distracted. irritable or hostile. frequently hyperactive. family & interpersonal) has been shown to reduce relapse rates. loosening of (usually thought blocking or poverty of associations). There is risk of suicide is unknown. Most severely depressed pt’s lack ~75% are assaultive or threatening. talkative. though ~50% deny May be euphoric. Hallucinations can occur but are rare. Psychosis can occur (called MDD with 75% have delusions – mood congruent psychotic features). motivation / energy to act in an Pt’s may commit suicide but incidence impulsive way. schizophrenia . & hallucinations may also occur. Negativity is customary. sometimes requiring sedation. psychotherapy (psychoanalytical. Lithium is typically combined with mood stabilisers (sodium valproate or carbamazepine) Non-Pharmacological Rx (MDD & Bipolar Disorder) Electroconvulsant Therapy (ECT)  Not 1st line Rx. Pt’s unfit for anaesthesia. There is often diurnal variation of severity. Insight is often excessive (pt’s often Impaired judgement is the hallmark. Can be grossly psychotic and disorganised. raised ICP Psychosocial Therapy Psychotherapies may be used alone for Rx of some cases of MDD (especially cognitive-behavioural). Most are fully orientated Most are fully orientated with normal 50-75% have cognitive impairment memory.

Concise Textbook of Clinical Psychiatry. pp. Borderline ○ Dementia References 1. bones. Therapeutic Guidelines (2006). Other mood disorders eg. Mood disorders often occur simultaneously with substance abuse / dependence iii. Elsevier Ltd.hcn. Substance-induced Mood Disorder  Mood disorders caused by drug or toxins  Must be ruled out in patients with depressive or manic sx’s. tumours)  Chronic renal failure  Hypercalcemia (moans. Cyclothymic disorder > 3. Adjustment disorder with depressed mood ○ Moderate depression in response to clearly identifiable stress. Bereavement ○ Profound sadness secondary to major loss ○ Differentiate from MDD by absence of suicidal ideation or profound feelings of worthlessness ○ Usually resolves within a year but may progress to MDD vii. 173-199 2. propranolol. steroids) ○ Anxiety disorders with depression ○ Personality disorders eg. cerebrovascular disease. Mood disorder resulting from general medical condition  Cushing’s syndrome / disease  Thyroid disorders  Neurological disease (Parkinson’s disease. Clinical Medicin 5th Edn. Dysthymic disorder. Kumar & Clarke (2002). epilepsy. 1243-48 and response to medications. Sadock & Sadock (2004).au > . amphetamines. ‘Schizophrenia’. < http://etg. recurrent brief depressive disorder. < http://www. stones & abdominal groans) ii. pp. v. ‘Psychotropic agents’. minor depressive disorder. Psychotic disorders ○ Eg. Schizophrenia. which resolves as stress diminishes vi. course premorbid hx. Other mental illnesses ○ Substance-induced mood disorders (eg. cocaine. Schizoaffective Disorder ○ Mood incongruent psychotic features suggests schizophrenia ○ Rely on such factors as family hx.firstconsult.DDx (Mood Disorders) i. FIRSTConsult.

Acceptance: Person comes to accept the situation eg. Sx’s last <1month) Post-traumatic stress disorder (PTSD. it applies in general to many different grieving stages. irritable and angry and may displace their anger onto others and/or themselves. of a loved one. ii. cure) and will in return fulfil promises 4. iv. usually clear ≤ 1year Responds to reassurance and supports Not helped by antidepressants Depression Delayed onset Abnormal over-identification with deceased. That death is inevitable 2.Stress Reactions i. Ambivalence and unconscious anger towards deceased Depressive sx’s with suicidal ideation Self-blame is global. Grief / Bereavement Adjustment disorder Acute stress disorders (ASDs. Depressive Sx’s but without suicidal ideation Self-blame restricted to how deceased was treated. 3.  Abnormal grieving reactions may respond to CBT and antidepressants. Bargaining: Pt may attempt to bargain with others or God for something (eg. However. person thinks they are generally bad or worthless Usually evokes interpersonal annoyance or irritation Sx’s do not resolve and may worsen Does not respond to reassurance and pushes supports away Helped by antidepressants Mx:  Normal grieving requires no specific Mx apart form support and encouragement to ventilate feelings and accept them as normal. Depression: Pt shows clinical signs of depression either due to the current effects on their life or in anticipation of future effects 5. Shock and Description Initial shock. Anger: Grief vs Depression Bereavement / Grief Immediate onset (at least of process) Normal identification with deceased. iii. . Little ambivalence with deceased. Sx’s last >1month) Bereavement Definition: A ‘normal’ expression of grief or mourning from loss eg. denial: Pts become frustrated. followed by denial that anything is wrong. 1. 2 Elisabeth Kübler-Ross Stages of Grieving This staging series describes the typical reaction to death and dying of a patient who is told of a terminal illness. It follows a recognisable sequence of stages that last for ≤ 2 years. No global feelings of worthlessness Evokes empathy and sympathy from others Sx’s self-limited.

Blackwell publishing. Psychotherapy (eg. Lippincott Williams & Wilkins. . Crisis intervention: aimed at helping the person resolve the situation quickly through any means necessary (including hospitalisation) 3. Pocket handbook of clinical psychiatry. 3 rd edn. Katona C & Robertson M (2005).Adjustment Disorders Definition: Disproportional or excessive clinical sx’s (emotional or behavioural) that develop in response to an identifiable psychosocial stressor(s)  3 months of onset of the stressor. CBT): Rx of choice. 2. Clinical Features:  Anxiety  Autonomic arousal  Depressed mood *Dx should only be made when there are insufficient sx’s to justify a diagnosis of another specific anxiety or depressive disorder. Australia. 3rd edn. used to explore what the meaning of the stressor was & alternative ways of coping 2. Kaplan & Sadock (2001). Mx 1. Pharmacology: Same as for anxiety disorders References 1. Psychiatry at a glance.

Delirium ii. auditory or tactile) and illusions  Delusions  Disorientation  Memory (& attention) impairment  Illogical speech  Reversed sleep-wake cycle  Psychomotor disturbance DDx a. Schizophrenia & mania .  Usually acute and reversible. Dementia b. inappropriate and unpredictably behaviour. 30% of ICU & AIDS patients Very young and very old more susceptible to delirium Aetiology Delirium is a common pathway for any brain insult. language and attention. swinging conscious state)  Agitation or fear  Prominent hallucinations (visual. Seizure disorders  Intoxication or withdrawal from medications or abusive substances eg.Cognitive Disorders (Organic Brain Disorders)     Consciousness = A state of wakefulness with awareness of self & surroundings Sleep = state of normal mental and physical inactivity where the pt can be roused Stupor = an abnormal sleepy state from which the pt can be aroused by external stimuli. but may become irreversible. They include: i.or Hypoarousal (ie. usually accompanied by global disturbances in cognitive function. renal failure. Epidemiology 10% of all hospitalised patients. Delirium (Acute Brain Syndrome) Definition:  Characterised by an impairment of consciousness. judgment. Dementia  Dementia of Alzheimer’s type (DAT)  Vascular dementia i.  Generally associated with emotional lability. Cardiac failure. Major causes include:  Systemic disease eg. Catatonic and depressive stupor Confusion = state of altered consciousness in which the subject is bewildered and misinterprets his or her surroundings The cognitive disorders are characterised by severe impairment in cognitive functions such as memory. ETOH withdrawal Signs / Sx’s:  Depressed conscious state  Hyper. SIRS  CNS disease eg. hallucinations / illusions. applied vigorously or repeatedly Eg.

social behaviour and motivation Epidemiology:  Affects 10-20% of people aged > 65 years  Increasing age is the biggest risk factor  The majority of cases are due to Alzheimer’s disease Aetiology:  Alzheimer’s disease (60-70% of cases)  Vascular disease  Head trauma  ETOH . U&E’s. LFT. Dissociative disorders: may show spotting amnesia but lack global cognitive impairment & disrupted sleep patterns Course & Prognosis Course is usually rapid with sx’s receding 3-7 days after the cause is treated. If cause remains unknown. but use with caution with cardiac conduction problems  BZD’s:  Diazepam 5-10mg PO (do not give IM as absorption is poor and erratic)  Midazolam 2.5-5mg IM (avoid IV due to risk of respiratory depression) Use BDZs If the most prominent symptom is Anxiety OR If agitation is not controlled with haloperidol BUT:  In patients with significant respiratory depression avoid all BZD’s  Because of the potential of BDZ’s to impair hypoxic respiratory drive. Dementia (Chronic brain syndrome) Definition:  An acquired. full medical work up should be performed immediately (FBE. lumbar puncture if indicated) iii. ii. Find the cause: Delirium is a Medical ER and the cause must be identified as rapidly as possible. CT of head. Agitation:  Antipsychotics:  Haloperidol 1. Rx the underlying cause iv. Sx resolution may take 2 weeks. urinalysis. 12-month mortality of 50%. use low flow rates if O2 is required used  Monitor vital signs closely during and after giving all sedatives  Use flumazenil if necessary to reverse the BZD effect.5-10mg PO or IM. 3-month mortality rate of 20-33%. ii. ECG.c. Mx i. In some cases the delirium may spontaneously clear. ESR. generalised and often progressive loss of cognitive function that does not affect the level of consciousness  Often associated with deterioration in emotional control.

  Huntington’s and Parkinson’s disease HIV infection .

’s have a superimposed delirium Course & Prognosis  Generally. subdural haematoma. and eventually become incontinent of faeces and urine  15% of dementias are reversible eg. hypoxia) and cognitive impairment depends on how soon the cause is treated Mx Rx is generally supportive. Dementia of Alzheimer’s Type (DAT)  Progressive dementia in which all known reversible causes have been ruled out  Most common cause of dementia (50-60% of all dementias)  5% over the age of 65yrs  RF’s include: female. purposeful movements without any sensory/motor impairment) – Agnosia (ability to recognise sensory stimuli) – Abstract thinking  Marked changes in personality. 1st degree relative with DAT (<40% have family Hx). B12 deficiency. uraemia. with some areas intact ○ Rx: Identify and prevent further CVA’s . Age-related Cognitive decline (Normal ageing) b. affect and behaviour can occur  Hallucinations (20-30%)  Delusions (30-40%)  Sx’s of depression and anxiety (40-50%) Tasks such as drawing & labelling a clock face and counting backwards from DDx a.Signs  Defect continually affects all higher cognitive functions – Memory (especially short term) – Planning & organising – Aphasia – Apraxia (ability to carry out familiar. the course is chronic and progressive  Often cognitive impairment is worse at night (‘sun-downing’)  As condition progresses. Depression (‘Pseudodementia’)  May present with many features of an cognitive impairment. Delirium / Acute Brain Syndrome  Also characterised by global cognitive impairment. Agitation can be treated with low dose antipsychotic. Avoid BZD’s and barbiturates as they worsen cognition. and most demented pt. CVA’s ○ 2nd most common cause of dementia (15-30% of all dementias) ○ Cognitive impairment may be patchy. slowed thinking and lack of spontaneity c. they may forget familiar places and people. Vit. head trauma. Down’s syndrome associated  Mean survival is 8yrs post-Dx  Rx: Anticholinesterases are used to slow cognitive decline. Hypothyroidism. especially with memory. but do not alter the underlying disease process Vascular Dementia ○ Dementia resulting from cerebrovascular disease ie.


personality changes Moderately disrupted Possible Yes No Mini-Mental State Examination  A screening tool – validated. but not diagnostic  Limited to coverage to parietal and frontal lobe functions  Subject to effects of culture and education  ‘Ceiling Effect’ – Can be difficult to use for screening because of the lack of difference in scores b/w those with dysfunction and those without . irritable Hallucinations common (esp. Insidious Months Years Pseudodementia (Depression) ≥ 2 weeks Gradual Normal Slowed Depressed. irritable No abnormalities Fluctuating but overall decreased Impaired Very Poor Normal Decreased Intact Less impaired Disorganised Impaired Highly disrupted Less disrupted Intact Decreased/Poor Slowed. visual). sad.Summary Onset: Duration: Psychomotor: Affect: Perception: Thought: Level of Consciousness: Orientation: Attention: Cognition: Sleep cycle: CT/EEG abnormalities: Delirium Dementia Sudden (acute) Days  Weeks Retarded. illusions Labile but not usually anxious Hallucinations less common (except ‘sundowning’) Delusions Delusions Mood-congruent delusions possible Anxious. agitated or mixed Slow. reliable.

v. iv. persistent and excessive anxiety about actual circumstances. Characterised by generalised. ii. (Also known as Social Anxiety Disorder). An irrational fear of public or social performance situations where the individual will be exposed to unfamiliar people or under scrutiny. and where the pt is free of anxiety in b/w the discrete PA’s. inability to cope)  Existential: that anxiety is a response to profound nothingness in life to fill the void in existence and meaning. Both obsession and compulsions produce anxiety if resisted. and compulsions are typically designed to relieve the anxiety produced by . vi. The YerkesDodson performance/anxiety curve illustrates that anxiety is beneficial up to a point beyond which performance deteriorates. events or conflicts lasting >6 months.  Psychoanalytic: Freud said the unconscious fear of loss / sense of danger threatens to break through to the conscious. The obsession is a mental event. images. producing anxiety. outside the home. learned behaviour from parents (eg. An irrational fear or an object where exposure (or anticipated exposure) causes massive anxiety. GABA causes CNS hyperactivity.  Cognitive-Behavioural: Classical conditioning to a specific stimulus (eg. PA’s tend to recur 2-3 times /week. Px is good-excellent with Rx. whereas the compulsion is a behaviour. Px*: Sx’s may diminish as pt gets older. 5-HT causes anxiety. Excellent Px with Rx. Sx’s may fluctuate. Px*: May worsen or spread w/o Rx. Agoraphobia is the most resistant of all phobias however. Characterised by intense resistance to leave the home. iii. impulses or thoughts (obsessions) and subsequent repetitive patterns of behaviour (compulsions). Aetiology of Anxiety Disorders  Biological: Sympathetic N/S hyperactivity & Noradrenaline release. but 2° depression may develop especially if GAD goes w/o Rx. i. It may occur alone or be a/w agoraphobia. Panic disorder ± Agoraphobia Generalised Anxiety Disorder (GAD) Phobias (Phobic disorder) Social anxiety disorder Obsessive-Compulsive Disorder (OCD) Post-Traumatic Stress disorder (PTSD) Panic disorder Agoraphobia GAD Phobias Social Phobia OCD Description Characterised by recurrent and spontaneous panic/anxiety attacks (PA’s). in public places or anywhere where escape / help could be difficult in the event of a PA. Px*: Remissions & exacerbations. Fear of being in open spaces. phobias). By far the most common phobia. Typically a PA will only last a few minutes. Involves recurrent intrusive ideas.Anxiety Disorders Anxiety is a state characterised by feelings of dread and accompanied by physical signs & sx’s of hyper-autonomic nervous system function. DSM: ≥ 3 PA’s in a 3 week period where there is no discernible danger to the pt.

DSM: Sx’s ≥1month = PTSD. Sx’s include reliving the event in dreams and waking thoughts (flashbacks).2 A pt with OCD usually has insight ie. twitching. *Course is chronic for all anxiety disorders. Physical Signs:  Autonomic hyperactivity  Tachycardia. In these disorders. feeling shaky  Fatigability Physical Sx’s: ○ “Butterflies in stomach” ○ “Lump in the throat” / Difficulty swallowing or choking ○ Chest pain ○ Dizziness. DSM: Obsession or compulsions cause marked distress. persistent anxiety with autonomic sx’s and numbing. palpitations  Sweating  Flushing & pallor  Cold hands  Diarrhoea  Dry mouth (xerostomia)  Urinary frequency  Pupil dilatation  Hyperventilation. Px*: Trauma is re-experienced for several years. Headache. Px with Rx is fair but some cases are refractory to all Rx modalities. Most common obsession = Cleanliness (43%). ≥4 of the following must be present for classification as a PA. realises the irrationality & absurdity (ego-dystonicity) of the obsession & compulsion. avoidance of reminders. Backache ○ Paraesthesias ○ Concentration ○ Hypervigilance ○ Insomnia ○ Libido Psychological Sx’s:  Feeling of impending doom / dread  Derealisation (the experience of the world or people in it seeming lifeless)  Depersonalisation (being detached from oneself)  Fear of ‘going crazy’. DSM Signs & Sx’s for Panic attacks & Anxiety disorders *A PA is a Sx not a Dx. Px*: Waxing and waning of sx’s. anxiety is produced by an extraordinarily stressful event. Sx’s <1month = Acute stress disorder. Compulsions may actually anxiety & not always be realistically connected to the obsession. Px is worse with +ve past psychiatric hx. losing control or dying . Most common compulsion = Hand-washing (85%). Dyspnoea  Muscle tension  Trembling. or take >1hr/day. but still feels ‘helpless’ to resist. social dysfunction. Often recalls facts without affect.PTSD the obsession.

including childhood - - Panic Disorder GAD Phobias Nb: 1° = 1st Degree. MZ = Monozygotic. early adulthood 25% of 1° relatives affected Concordance in MZ twins > DZ twins 80-90% concordance in MZ twins.Epidemiology Lifetime Prevalence ♂:♀ Ratio Age at onset Family Hx Twin Studies 1. 1015% in DZ twins 10% *Most common anxiety disorder 1:2 Late childhood May run in families - OCD 2-3% Even Adolescence or early adult life 35% in 1° relatives. DZ = Dizygotic . Concordance in MZ twins > DZ twins PTSD 1-3% 30% in Vietnam veterans 1:2 Any age. a/w Tourette’s syn.5-4% Even Late 20’s 50% of pt’s have one affected relative 3-8% 1:2 Variable.

Cerebral neoplasms. Medical & neurological conditions  Hypoxia  Endocrine disorders eg. cocaine. and 20-30% of primarily anxious patients also experience depression1  Bipolar I Disorder  Massive anxiety may occur during a manic episode Psychotic disorders  Schizophrenia  Schizophrenic patients may be anxious and have severe obsessions in addition to or preceding the outbreak of hallucinations or delusions  Atypical psychosis (psychotic disorder not otherwise specified)  Massive anxiety is present. . Phaeochromocytoma  Inflammatory disorders eg. SLE.  + Many many more Substance-related disorders  Anxiety often associated with intoxication (especially caffeine. epilepsy. hallucinogens) and withdrawal states. encephalitis.DDx Mood disorders  Depressive disorders (MDD)  50% of MDD exhibit anxiety or obsessive brooding. amphetamines. etc. haemorrhages. Rheumatoid arthritis  Malignancy  Neurological disorders eg. in addition to psychotic features Adjustment disorder with anxiety  Patient has a history of psychosocial stressor ≤ 3 months of onset. migraine. MS.

even w/o depressive sx’s)  Paroxetine (Aropax) and Sertraline (Zoloft) are currently approved but others may be tried  Indicated for all anxiety disorders except phobias. secondary gains of the sx’s. References 1. Pocket handbook of clinical psychiatry.  Supportive Psychotherapy  Use of psychodynamic concepts to promote adaptive coping by promoting adaptive defences and discouraging maladaptive ones. initially a transient anxiety may occur  Tricyclic Antidepressants (TCAs) (2nd Line Rx)  Imipramine (Tofranil) is the TCA of choice  Doses are typically higher for panic than for depression  Irreversible Monamine Oxidase Inhibitors (MAOIs) (2nd Line Rx)  Phenelzine (Nardil)  Risk of hypertensive crisis & fatal intracranial bleeding with consumption of foods containing tryptophan or tyramine. Lippincott Williams & Wilkins. Blackwell publishing. Psychiatry at a glance. Kaplan & Sadock (2001). Immediate Mx of PA  Isolated PA’s should be treated with non-pharmacologic means & all other medical causes should be ruled out (eg. 3 rd edn. i. iii. Short-term Mx  SSRIs (1st Line Rx. used to treat residual or anticipatory anxiety (~30mins to enter blood stream)  BZD usage has largely been replaced by newer SSRIs but Alprazolam is particularly good and can be used in combination ii.  Breathing techniques: Deep slow breathing or Re-breathing in a paper bag (Arterial CO2 & Sx’s)  Benzodiazepines  eg. etc. Oxazepam (Serepax) PO. TCAs. Diazepam (Valium) 2-5mg PO. Long-term Mx  Continue pharmacological Rx as required  Cognitive-Behaviour Therapy  Effective in disorders where thoughts cause behaviour eg. 2. Australia. can manifest as symptomatic behaviour  This includes the subconscious meanings of their anxiety. OCD  Insight-Orientate Psychotherapy  Goal is to insight into psychological conflicts that. Alprazolam (Xanax) PO  Not usually for Rx of acute attacks. or with co-administration of narcotics.Mx of Anxiety Disorders Rx will vary depending on the anxiety disorder. whereas the other disorders are usually combined with pharmacology. Phobias and PTSD are best treated with psychotherapy alone. AMI). Katona C & Robertson M (2005). symbolism. . 3rd edn. or other MAOIs. if unresolved.

actually experiences physical sx’s as an expression of unconscious conflict  Factitious disorder = conscious deception but for unconscious secondary gains apart from assuming the sick role  Malingering = conscious deception for conscious secondary gains . v. 2. iii. beliefs may progress to delusions. Morbid fear or belief that one has a serious disease even though none exists. GIT. Somatization disorder Conversion disorder Hypochondriasis Body dysmorphic disorder Pain disorder Epidemiology  ♂<♀  Generally more common in low-socioeconomic & low-education groups  Less seen in psychiatric institutions. SSRI’s effective in 50% Psychotherapy useful Pain disorder A preoccupation with pain in the absence of physical disease to account for its intensity. much more common in medical wards and GP surgeries Definition Multi-system complaints (pain. neuro) that recur over several years & are not explained by any known medical condition. Factitious vs. Body dysmorphic disorder Imagined belief (not of delusional proportions) of a bodily defect. waxes and wanes Chronic course. Tends to recur. Malingering  Somatoform disorder = pt. ≥ 1 neurological sign or sx a/w psychological conflict or need. Psychotherapy (Insight. pseudoseizures. and they are significant enough to cause distress and functional impairment. Unnecessary interventions common. CBT) Course & Px Chronic course. episodes in b/w are sx-free. Px: Unknown Px: Variable Somatoform vs. i. iv. Px: Excellent (except in chronic cases) Chronic course with remissions. ii. Psychotherapy and counselling Somatisation disorder Conversion disorder Hypochondriasis Must find all medical causes (medical disorder eventually founding 25-50% of cases). BZDs for anxiety Antidepressants for obsessive ruminating about sx’s Psychotherapy (Insight. ataxia. Insight or Supportive psychotherapy useful. Mx 1. few remissions. These patients’ physical sx’s are a manifestation of their mental illness. Depressive sx’s common. CBT) Anti-anxiety & antidepressants. sexual. Px: Poor to fair.Somatoform Disorders Somatoform disorders are distinguished by physical sx’s that cannot be explained by a medical or other psychiatric condition diagnosed in the patient. blindness & other neurological signs/sx’s. Px: Fair to good. Pt’s present with paralysis. Avoid psychotropics as pt’s often become dependant.

Contact child welfare services if disorder is in a parent Malingering Definition: Voluntary and conscious production of physical or psychological sx’s in order to accomplish a specific goal / secondary gain (eg. delusions. pain. Psychosocial history usually reveals some area with a defined goal (where secondary gain occurs). insurance payments. be admitted to hospital). bizarre behaviour  Fabricating stories of stress & extravagant lies that the patient may believe  Stories of substance abuse Course & Px  Course is typically chronic  Substance abuse risk is high over time  Risk of death from multiple surgical procedures over time Mx    Avoid unnecessary tests & procedures and confront pt about diagnosis of a Factitious disorder and feigned sx’s. Psychopharmacological therapy is useful for associated anxiety or depression. avoid jail term). seizures  Intentionally putting blood in faeces or urine  Artificially raise body temperature  Take insulin to lower BSL Psychological signs & sx’s:  Intentionally production of psychiatric sx’s – hallucinations. Any other gain is unconscious (ie. Clinical Presentation Physical signs & sx’s:  Nausea. Help provide ways of managing the stressor. Mx Pt should be monitored as if real disease were present. depression. Appropriate Mx of substance abuse. They are easily irritated if the doctor shows any scepticism to the history. Clinical Presentation Patients may have vague or poorly localised sx’s that are described in great detail. Identify areas of secondary gain and allow pt to ventilate.Factitious Disorders Definition: Where patients consciously produce physical or psychological sx’s in order to assume the sick role (and in most cases. vomiting. . but no Rx should be offered. no external incentive).

driving) 3. Personality disorders. using and recovering from the substance Withdrawal Syndrome ○ Agitation ○ Sweating & Fever ○ Musculoskeletal pain ○ Abdominal cramps ○ Diarrhoea. schizophrenia ○ Psychosocial stress Neuropharmacology ○ ETOH is a depressant that produces somnolence and neuronal activity. Withdrawal sx’s on cessation 3. Great deal of time / effort is spent on obtaining.Substance Abuse Abuse (DSM) 1 or more of the following within a 12 month period: 1. Incidence of abuse / dependence increases with: ○ FamHx of alcoholism (4 fold risk) & depression ○ Race eg. tolerance to ETOH causes tolerance to the other agents despite not actually been exposed). ○ These agents are cross-tolerant with ETOH (ie. Substance use is continued despite knowledge of adverse physical or psychological problems 7. Substance taken for longer or in larger amounts than expected 4. nausea and vomiting ○ ○ ○ ○ ○ Tachycardia piloerection (goose-bumps) Shivering or trembling Increased blood pressure Seizures Alcohol (ETOH) Aetiology Aetiology is very multifactorial. Persistent desire / failed efforts to cut down 5. NMDA) ○ ETOH is potentially lethal when taken in combination with any agent from this class eg. Low incidence in Asians ○ Concurrent psychiatric disorders eg. Tolerance (dose for same effect) 2. ○ It is thought to production of opioid-like alkaloids as well as act on many other receptor pathways (eg. Recurring substance related legal problems 4. barbiturates and carbamates. Recurrent use causing failure to fulfil major 2. Continued use despite recurrent social or interpersonal problems Dependence (DSM) At least 3 of the following occurring within a 12month period: 1. Hx Cut down before (tried)? Annoyed when others have suggested you cut down? Guilty about amount you drink? . Impaired social or occupational functioning 6. It can be categorised with the other sedative-anxiolytics such as BZD’s. Recurrent use in physically hazardous situations (eg. BZD’s.

you can use the AUDIT questionnaire (8-14 is risky of harmful usage. Detoxification and Rx of withdrawal sx’s 2.  Decreases craving for ETOH by blocking release of Drinking rate (66%).Eye-opener to get the day started? Alternatively. endogenous opioids / receptor blockade Very few SE’s & No  One tablet per day. used for 612mths. withdrawal state. so use is temporary only  Naltrexone (ReVia) Both 1st line. 1.  Decreases craving by other receptor system blockade . intoxication is more pronounced with BAC is rising rather than falling Liver biochemistry  GGT: measure of recent ETOH consumption (also with DM)  AST & ALT: if raised. Al-Anon is for the patient’s family 3. Patient must see that they have a problem. up to 3 days per wk Females ≤ 4 per day. Psychopharmacology  Disulfiram (Antabuse)  Inhibits aldehyde dehydrogenase causing accumulation of acetaldehyde  Causes ETOH to taste terrible & ingestion to result in flushing. Compliance is good. 50% have ‘fatty liver’. Psychotherapy: Family Therapy is particularly useful 4. Low Risk Short-term harm risk: Males ≤ 6 per day. Alcoholics Anonymous (AA) and Al-Anon  AA is for the patient. nausea and vomiting  Compliance is the biggest problem. up to 3 days per wk Long-term harm risk: Males ≤ 4 per day ≤ 28 per week Females ≤ 2 per day ≤ 14 per week Medium Risk High Risk 7-10 per day 11+ per day 5-6 on any day 7+ per day 5-6 per day 29-42 per week 3-4 per day 15-28 per week 7+ per day 43+ per week 5+ per day 29+ per week Ix’s       FBE: Macrocytic anaemia Blood Alcohol Concentration (BAC)  Rapidly rising BAC correlates with degree of intoxication. >14 indicates dependence). Insight is the first critically important step but can be difficult to achieve.  Acamprosate (Campral) Cheap (relatively). All biochemistry will be deranged in decompensated cirrhosis Liver function tests (LFT’s)  Serum albumin and Prothrombin Time (PT) are the best indicators Ultrasound (Dx cirrhosis) Serum -fetoprotein: Marker of HCC Mx The goal is prolonged maintenance of total abstinence.

Buprenorphine (partial-agonist) + Naloxone (Suboxone) Long acting oral opioid agonists prevents the development of withdrawal sx’s. 3 tablets per day Heroin Neuropharmacology Opioids affect opioid receptors. or combined with stimulants IV (‘speedball’). Home Detox Detox cold turkey. Abstinence programs Family help ± Community services Not necessarily ‘at home’ eg. Route Multiples routes. Blocks opiate effects for those committed to abstinence. IV (heroin). . Substitution programs 5. Smoked (opium). has a faster onset of action and cross the blood-brain barrier faster than morphine. diureses & sedation  -opioid receptors: mediate analgesia Heroin is more potent. inhaled (snorted). and blocks the euphoric effects of heroin if relapse occurs. Risk of OD due to tolerance.4mg IV or IM every 2-3mins up to 2mg Success rates 5-10% abstinence Mortality ~2-3% per year 5-10% abstinence (or less) 50% pt retention at 1year 25% pt heroin cessation at 1year 4-fold reduction in mortality Very poor retention rates. constipation & dependence  -opioid receptors (kappa): mediate analgesia. more addictive. Mx (OD) Naloxone (Narcan) 0. Naltrexone (ReVia) PO Pure long-acting opiate receptors antagonist. craving. Methodone (full-agonist) b. IV use. respiratory depression. as well as dopaminergic systems. Withdrawal centres 3. Nothing Description No interventions 2. Clinical Features         Signs CNS depression GIT motility Respiratory depression Nausea + vomiting Bradycardia & Hypotension Slurred speech Pupillary constriction (‘pin-point pupils)’ Seizures ○ ○ ○ ○ ○ Sx’s Euphoria (‘total body orgasm) Swinging anxiety / tranquillity Attention & memory Drowsiness Psychomotor retardation Mx (Long Term) Mx Option 1. travel Adjuvant BZD’s effective a.  -opioid receptors: mediate analgesia. residential detox 4.

hepatorenal and cerebral damage. glue. petrol)  Initial euphoria is followed by drowsiness  Psychological is common but not physiological  Toxic effects: Cognitive impairment.)  Cocaine Sedatives & Hypnotics  Barbiturates  Benzodiazepines (BDZ’s) Others  Solvents (eg. It reverses opioid effects of CNS & respiratory depression within 2 mins (IV).  Naloxone is a fast acting opioid-receptor antagonist. impaired consciousness and psychosis . An acute withdrawal syndrome may occur post-adm in dependent patients Other Drugs Hallucinogens  Lysergic acid diethylamide (LSD)  Produces physiologic & psychologic effects but not dependence  Magic mushrooms (Psylocibin)  Have effect similar to but less intense than LSD  Ecstasy (MDMA):  Synthetic amphetamine analogue  Has mixed stimulant and hallucinogenic properties Stimulants  Amphetamines (speed. polyneuropathy  Phencyclidine (PCP or ‘angel dust’)  Usually smoked  Effects include euphoria. crystal meth. peripheral analgesia.

eccentric. believe that everyone is out to get them / bring them down Often hostile. pt seeks to alter the environment rather than self)  Traits are held rigidly  Underneath the protective defensive mechanisms lies anxiety Dx   Dx requires a Hx of long-term difficulties in social and occupational spheres By definition PD cannot be diagnosed in 16yrs old as ‘personality has not been formed’ Cluster A Paranoid PD Schizoid PD Schizotypal PD Cluster B Histrionic PD Narcissistic PD Antisocial PD Description Odd. and introverted Suspicious and mistrustful. Similar to narcissism but less body-orientated. in ♂. Personality Disorder (PD): When personality traits are rigid. Appear strange to others. dramatic. Pervasive pattern of grandiosity & overconcern with issues of self-esteem. very attention seeking. Gets bored easily so jumps from thing to thing.Personality Disorders Personality: Described as a person’s characteristic configuration of behaviour response patterns in ordinary life. obsessed with body and image. Person is hyper-dramatic & extraordinarily seductive but frigid & immature. Divinely right. Maladaptive behaviour where the pt doesn’t Defences Fantasy (create imaginary worlds and friends) Projection (unacknowledged feelings are attributed to others) A/w tendency for psychotic thinking Dissociation (unpleasant affects are repressed or replaced with pleasant ones) Denial Splitting (others seen as all good or all bad) Acting out (wishes or conflicts are expressed in action without awareness of the idea or affect). in OCD)  Traits are alloplastic. emotional & erratic “Hollywood” / Paris Hilton / Self-centred. maladaptive and produce functional impairment and subjective distress. outward. Explode easily over nothing if they are crossed. Love is the hardest part of success Connections with ‘magical thinking’ and reliance on superstition to resolve conflict. Stems from being rejected as “dad’s little girl” when she hits puberty. . Features  Traits are pervasive and persistent  Traits are ego-sytonic (ie. not autoplastic (ie. often bigots High prevalence in armed forces High propensity to develop psychosis (schizo) ‘Space cadet’. multiple oddities Explosive. have ‘shadow r/ships’ where the other fulfils their needs.  in ♀. irritable or angry. Attracted to solo / powerful positions. acceptable to the ego). aloof and vague Lives an isolated lifestyle. not ego-dystonic (eg. a totality that is usually stable and predictable.

with difficulty with disagreement. etc. Deep seeded anger is communicated by “forgetting” or “omitting” things to harm others. hates to confront or discuss conflict (esp. emotional). Procrastination over minute details. self-blaming and introverted.  in ♀. Strongly a/w young sexual abuse. Incapacity to feel guilt. Self-image / worth problems so will follow influence of others. Easily hurt and sensitive to rejection. fearful and ‘neurotic’ Shy or timid personality. rules & regulations) and inflexibility predominate. Has a sense of self but is submissive. anger.  in ♀. Splitting invariable. Very high prevalence in jails Pt fluctuates between psychosis and reality Self-harm (to ‘see they are alive’) is the hallmark ie. Pt pain is intense Anxious. very anxious. Passive. always does what the other wants. orderliness (inc. socially withdrawn but desires social involvement.Borderline PD Cluster C Avoidant PD Dependant PD Obsessive compulsive PD PassiveAggressive PD recognise the rights or feelings of others. Lack self-confidence and intolerant of being alone. Likes to get along with others but cannot cope with anger (sublimation). Isolation (facts are recalled without affect) Passive-aggression (aggression towards others is expressed indirectly through passivity) Hypochondriasis (where physical sx’s / illnesses are exaggerated as a means of evading guilt. ~50% will suicide. valproate and carbamazepine) can help episodic behavioural dysfunction . Unstable and intense r/ships very common. sexual dysfunction common Not social. responsibility. acting out.) Mx Psychotherapy choice is dependant on the PD:  Group therapy  CBT  Dialectical Behaviour Therapy (DBT) for Borderline PD Pharmacological:  Antipsychotics may be useful for cognitive sx’s  MAOIs may be helpful in Borderline PD (Rx mood)  Mood stabilisers (Lithium. blames others. Perfectionism.

o are highest risk group 2. Hospitalise if unsure (even in ER) Relieve any immediate distress to the patient  Make a ‘No Harm Contract’ with patient  Rx agitation with Haloperidol or BZD’s if required  Commence Rx of any underlying illness eg. Assess suicidal plans “Any thoughts of suicide?”:  Detailed action plan  Means to accomplish suicide (eg. Medium or High)  High risk pts should not be left alone. Depression Longer-term:  Continue Rx of psychiatric illness eg. Assess emotional state  Do you think things will ever get better?  Do you feel like a burden on people?  Does anything give you pleasure / is anything stopping you? History Taking (Risk Factors): 1. Male + Caucasian + >45y.Risk Assessment Presentation Typically sad. HIV. malignancy or chronic pain)  Physical or sexual abuse 5. tablets) & Intent not to get caught  Finalisation of affairs eg. Firearms. Recent loss / Anniversary of important loss 3. ECT if required for depression  . depressed and with evidence of self-neglect. Beware of those who appear bright and elated – they may ready to complete their suicide plans. Clinical Assessment Current state: 1. PHx of:  Suicide attempts or self-harm (para-suicide)  Chronic physical illness (especially CNS disorders. FamHx of suicide 6. Will 2. Poor social support Mx Immediate:  Assess risk (Low. Psychiatric disorders:  Mood disorders  Psychotic disorders (Schizophrenia & Schizoaffective)  Personality disorders (especially Borderline)  Drug & ETOH abuse / dependence 4.

support services & Psychotherapy (CBT. Family therapy) . Counselling.

nausea & myalgia (common): Last the day of the treatment  Cognitive deficits (post-ECT delirium) . It is known that the treatment has a positive effect on inducing brain neurotransmitters. excitement) of motor system  Typically occurs in catatonic schizophrenia. NMS e) Rapid Rx response eg. Bipolar Disorder. The most common treatment is high-dose right unilateral therapy with electrodes over the right temporal region and near the vertex. especially antiepileptics (as they raise seizure threshold)  Pt put under GA and given muscle relaxants  During:  Seizure is induced for typically ~30secs SE’s:  Headache. stupor) or overactivity (c. a bilateral approach is used Indications: a) Acute mania or psychosis (especially if psychosis is extreme) b) Severe depression  Postnatal depression  Psychosis  Melancholic depression refractory to other Rx  Where it has been efficacious in the past c) Schizophrenia  Refractory to other Rx  Where it has been efficacious in the past d) Catatonia  Extreme under. the mechanism of action remains unclear.Electroconvulsive Therapy (ECT) Mechanism: While the effectiveness of ECT has been shown. Less commonly. brain tumour) Relative: ○ Severe HTN and/or Aneurysms (BP during tonic-clonic phase) ○ Recent myocardial infarction (AMI) ○ Bradyarrhythmias (HR during shocks) ○ Pacemakers (low risk of electrical damage to pacemaker) ○ Osteoporosis (risk of # during tonic-clonic phase) ○ MAOI or TCA use within the last 14days Procedure  Before:  Cessation of all psychotropics. acute suicidality f) Medical conditions  Neuroleptic malignant syndrome (NMS)  Parkinson’s disease Contraindications Absolute:  Raised ICP (or any condition a/w raised ICP eg. Depressive stupor leading to self-neglect. but can occur in other conditions eg.(c.

gov. less evidence for the 1st trimester References: 1. compared to medications which can take weeks to show effect  Pregnancy: Can be used in confidence in the 2nd and 3rd trimesters. but this subsides during the day  Short term memory loss: Usually fully regained in the weeks following completion of the course of treatment Nb. and this may improve post-ECT Cx’s:    Risks undergoing GA Long-term memory loss (rare) – Increased risk with bilateral ECT Medical Cx’s Ruptured aneurysm Course of ECT ○ ECT involves a series of treatments to achieve optimum outcome ○ Typical course = 3 times / week.qld. Health < http://www.pdf > . with a total number averaging between 6-12 ○ The number of treatments will vary according to the individual Benefits of ECT:  Clinical evidence shows that ECT will produce a substantial improvement in around 80% of patients with severe major depression. Depression is associated with cognitive impairment also. Confusion & disorientation (common) in the hour after  Speed of efficacy: ECT can show clinical effect after a few treatments. QLD Govt.