deck_8091483 Flashcards

1
Q

<p>What is the general approach to dealing with a patient with acute behavioural disturbance</p>

A

<p>1. Maintain safety and calm situation; easy access to exits, maintain some distance between you and the patient<br></br>2. Verbal de-escalation and early negotiation (calm voice, sit with patient, offer food/drink, let them voice their concerns, offer oral medication (diazepam PRN or olanzepine once)<br></br>3. Show of force; bring large number of staff<br></br>4. Physical restraint by trained team<br></br>5. Chemical restraint (IV access preferred, give diazepam/midazolam/droperidol or olanzepine, if need to give IM consideer midazolam, olanzapine)</p>

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2
Q

<p>Appearance </p>

A

<p>Physical state: how old do they appear? Do they appear physically unwell? Are they sweating? Are they too thin or obese? EtcClothes and accessories: Are their clothes clean? Are they wearing the same clothes since when you last saw them? Are clothes appropriate for the weather/circumstance? Is the patient carrying strange objects?Self-care &amp;amp; hygiene: does the patient appear to have been neglecting their appearance or hygiene (eg. Unshaven, malodourous, dishevelled)? Is there any evidence of self-harm (eg cuts to wrists/forearm)?</p>

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3
Q

<p>BEHAVIOUR </p>

A

<p>Abnormal movements: tremors, tics, twitchesHow the patient is acting: Are they relaxed/ suspicious/ aggressive/ fearful/ catatonic?Psychomotor abnormalities: retardation (slow, monotonous speech, slow/absent body movements), agitation (inability to sit still; fidgeting, pacing, hand wringing, rubbing/scratching skin or clothes)Rapport: What is their attitude towards you? Do they make good eye contact? May be described as cooperative, cordial, uninterested, aggressive, defensive, guarded, suspicious, fearful, perplexed, preoccupied, disinhibited, etc</p>

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4
Q

<p>Parkinsonism </p>

A

<p>drug-induced signs are most commonly a reduced arm swing + unusually upright posture while walking. Tremor + rigidity are late signs, in contrast to idiopathic parkinsonism</p>

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5
Q

<p>Acute dystonia </p>

A

<p> involuntary sustained muscular contractions or spasms</p>

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6
Q

<p>Akathisia</p>

A

<p>subjective feeling of inner restlessness and muscular discomfort, unable to sit still</p>

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7
Q

<p>Tardive dyskinesia</p>

A

<p>rhythmic, involuntary movements of the head, limbs and trunk, especially chewing, grimacing of the mouth and protruding, darting movements of the tongue</p>

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8
Q

<p>Bradykinesia </p>

A

<p>slowness of movement</p>

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9
Q

<p>SPEECH</p>

A

<p> Rate: may be regular, may have pressure of speech (seen in mania), long pauses/hesitancy + poverty of speech(seen in depression)Tone: may be regular tonality, monotonousVolume: regular, increased or decreasedAlso comment on dysarthria (articulation difficulties), dysprosody (unusual speech rhythm, melody, intonation or pitch), stuttering, slurring</p>

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10
Q

<p>Mood</p>

A

<p>Refers to a patient’s sustained, subjectively experienced emotional state over a period of timeAssessed by asking the patient how they are feeling- Described objectively (your impression from the interview) and subjectively (their description of how they feel) Dysphoric: an unpleasant mood, eg. Depression, anxiety, irritabilityEuthymic: the mood is within the “normal” range, implying that mood is neither depressed nor elevated Expansive: the mood is more elevated than normal, but does not necessarily imply pathologyEuphoric: an intense feeling of well-being</p>

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11
Q

<p>AFFECT</p>

A

<p>A subjective feeling/emotional experience that is manifested by observable behaviours such as attitude, facial expression, tone of voice, etc.Affect is assessed by observing patient’s posture, facial expression, emotional reactivity(1) Changeability• Restricted – characterised by discernible decrease in range + intensity of expressions• Labile – characterised by rapid &amp;amp; abrupt changes , eg. Friendly + cheerful one minute and thenangry and belligerent the next for no apparent reason(2) Range = Normal/ increased/ decreased(3) Appropriateness = congruent/incongruent (discordance between speech and affect)(4) Intensity • Blunted – associated with marked diminuition in emotional expression• Flat – the normal signs of a broad range of affective expression are absent; voice may bemonotonous, face may be immobile/expressionless </p>

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12
Q

<p>THOUGHT FORM - Circumstantial </p>

A

<p>An inability to answer a question without giving excessive, unnecessary detail – differs from tangential thinking, in that the person does eventually return to the original point</p>

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13
Q

<p>THOUGHT FORM - tangential </p>

A

<p>Wandering from the topic and never returning to it nor providing the information requested</p>

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14
Q

<p>THOUGHT FORM - Loosening of association </p>

A

<p>characterized by discourse consisting of a sequence of unrelated or only remotely related ideas. The frame of reference often changes from one sentence to the next.</p>

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15
Q

<p>THOUGHT FORM - Neologisms </p>

A

<p>Creation of a new word, often consisting of a combination of other words, that is understood only by the speaker</p>

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16
Q

<p>THOUGHT FORM - Flight of ideas </p>

A

<p>A rapid shifting of ideas with only superficial associative connections between them that is expressed as a disconnected rambling from subject to subject and occurs especially in the manic phase of bipolar disorder</p>

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17
Q

<p>THOUGHT FORM - Thought blocking </p>

A

<p>Occurs when a person's speech is suddenly interrupted by silences that may last a few seconds to a minute or longer</p>

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18
Q

<p>THOUGHT FORM - preservation </p>

A

<p>Persistent repetition ofwords or ideas even when another person attempts to change the topic</p>

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19
Q

<p>THOUGHT FORM Echolalia </p>

A

<p>Echoing of another speech </p>

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20
Q

<p>THOUGHT FORM - Alogia </p>

A

<p>Poverty of speech, either in amount of content </p>

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21
Q

<p>Thought Content - Preocupations </p>

A

<p>over-valued or recurrent thoughts</p>

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22
Q

<p>THOUGHT CONTENT - obsessions </p>

A

<p>Distressing recurring unwanted thoughts </p>

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23
Q

<p>THOUGHT CONTENT - Delusions </p>

A

<p>A fixed false belief not accounted for by patient's cultural background </p>

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24
Q

<p>THOUGHT CONTENT - PARANOID DELUSIONS </p>

A

<p>The person/group is being attacked, threatened, harassed, endangered, deceived or persecuted </p>

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25
Q

<p>THOUGHT CONTENT - GRANDIOSE DELUSIONS </p>

A

<p>a delusion in which theperson has an exaggerated view of his/her ownimportance, power, knowledge, or identity</p>

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26
Q

<p>THOUGHT CONTENT - DELUSIONS OF REFERENCE </p>

A

<p>events/objects/otherpeople in the subject’s immediate environmentare seen to have unusual &amp;amp; special significance</p>

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27
Q

<p>THOUGHT CONTENT - IDEAS OF REFERENCE </p>

A

<p>similar to delusions ofreference but the beliefs are more shakeable</p>

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28
Q

<p>THOUGHT CONTENT - DELUSIONS OF CONTROL/ PASSIVITY EXPERIENCES </p>

A

<p>belief that the person’s feelings/ impulses/ thoughts/ actions are not his or her own, but rather are inserted by another</p>

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29
Q

<p>THOUGHT CONTENT - SOMATIC DELUSIONS </p>

A

<p>Relates to functioning of the body e.g being pregnant, rotting brain </p>

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30
Q

<p>THOUGHT CONTENT - NIHILISTIC DELUSIONS </p>

A

<p>false belief that self, part of self, others, or the world is nonexistent or ending</p>

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31
Q

<p>PERCEPTION</p>

A

<p>Determine whether the abnormal perceptions are genuine hallucinations, pseudohallucinations, illusions, or intrusive thoughts • Describe from which sensory modality the hallucinations arise – eg. Auditory, visual, tactile, olfactory, gustatory, somatic • Determine whether auditory hallucinations are elementary or complex • If complex – are they experienced in first person (audible thoughts, thought echo), second person (critical, persecutory, complimentary or command hallucinations) or third person (voices arguing or discussing the patient, or giving a running commentary) • It is also important to note whether the patient is responding to hallucinations during the interview, as evidenced by them laughing as though they are sharing a private joke, suddenly tilting their head as though listening, or quizzically looking at hallucinatory objects around the room</p>

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32
Q

<p>COGNITION </p>

A

<p>• Screened by checking orientation to person, place, time• Usually not formerly assessed unless you have time for an MMSE</p>

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33
Q

<p>INSIGHT </p>

A

<p>• Often described as good, partial, or poor – however usually patients lie somewhere on a spectrum and vary over timeKey questions to answer;- Does the patient believe they are unwell in any way? Do they believe they are mentally unwell?- Do they think they need treatment?- Do they think they need to be in hospital?</p>

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34
Q

<p>JUDGEMENT </p>

A

<p>- Reasoning regarding current important issues- Ideas about decisions or actions to be taken, including about current illness- Evidence from past judgements as clues to current thinking</p>

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35
Q

<p>MOA, Examples, positives and negatives of 1st generation/ TYPICAL antipsychotic medications </p>

A

<p>MOA - Block post synaptic D2 receptors in mesolimbic, mess cortical, nigrostriatal and tuberoinfundibulnar pathways EXAMPLES - Haloperidol (high potency) - Chlorpromazine (low potency) POSITIVES - inexpensive - injectable/ depot form - minimal metabolic side effectsNEGATIVES - Extrapyramidal SE - Not mood stabilising - Reduced DA in mesocortiyal pathway can induce negative side effects - Tardive symptoms in long term use </p>

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36
Q

<p>MOA, Examples, positives and negatives of 2nd generation/ ATYPICAL antipsychotic medications</p>

A

<p>MOA - Block post synaptic D2 receptors (less affinity than 1st gen) - Block 5HT2A on presynaptic dopamine terminals to reverse dopamine blockafe in some pathways EXAMPLES - Risperidone - Olanzapine - Quetiapine - Aripiprazole - Clozapine POSITIVES - Fewer EPS - Low tar dive symptom risk - mood stabilising NEGATIVES - Expensive - Metabolic SE !!! (increase wt, BGL, lipids, MetSy) - Exacerbation/ new onset obsession behaviour</p>

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37
Q

<p>Second generation antipsychotics adverse effects NOTE: see notes for specific SE of specific SGAs (table) </p>

A

<p>Common▪ Insomnia▪ Akathesia (very common!)▪ Headache▪ Sedation (esp Quetiapine and olanzapine)▪ Metabolic syndrome + weight gain▪ Cardiovascular- May increase the QT interval, increasing the risk of arrhythmia - orthostatic hypotension- some ↑ in VTE riskUncommon but Serious▪ Extrapyramidal Side effects - Dystonia- Akathesia- Pseudo-parkinsonism -Tardive Dyskinesia▪ Neuroleptic malignant syndrome (FARM symptoms)▪ Blood dyscrasias- anaemia, thrombocytopenia, neutropenia, agranulocytosis▪ New-onset or worsening obsessive-compulsive symptoms (clozapine)EXTRAPYRAMIDAL SIDE EFFECTS▪ highest with haloperidol, fluphenazine and trifluoperazine▪ lower with chlorpromazine, periciazine▪ Is dose dependant – so Reduce antipsychotic dose to avoid recurrent EPSENOTE: AKATHESIA= inner restlessness and a compelling need to be in constant motion, as well as by actions such as rocking while standing or sitting, lifting the feet as if marching on the spot, and crossing and uncrossing the legs while sitting</p>

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38
Q

<p>Clozapine - Indications, contraindications, receptor profile/MOA, adverse effects, interactions, patient counselling, monitoring (Antipsychotic) </p>

A

<p>INDICATIONS▪ Schizophrenia in people unresponsive to, or intolerant of, other antipsychotics (ie lack of satisfactory clinical response, despite the use of adequate doses of drugs from at least 2 groups of antipsychotics for a reasonable duration; or development of EPSE, including tardive dyskinesia)CONTRAINDICATIONS▪ Contraindicated in bone marrow disorders, drug-induced (including clozapine-induced) neutropenia or agranulocytosis (Neutropenia seems to be more common in children and adolescents than adults)▪ Severe Renal or Liver impairmentRECEPTOR PROFILE/ MOA▪ BLOCK 5HT2 to 90%▪ BLOCK D2▪ BLOCK M1▪ BLOCK D4(with high affinity related to plasma concentration)▪ BLOCK H1, alpha 1ADVERSE Common - Sedation ++- Hypersalivation ++ - Increase HR ++ - Constipation- Seizures - Pyrexia - Urinary incontinence Infrequent - Hepatitis ++- Myocarditis ++- Neutropenia ++- Angranulocytosis ++ - EPS ++- Eosinophilia - Priapism Rare - Cardiomyopathy ++- HTN- Myoclonic jerks - Interstitial nephritis - Fulminant hepatic necrosis Metabolic ▪ ↑↑ BGL. ↑↑ Lipids, ↑↑ weight▪ ↑↑ Risk of developing T2DM (must assess before + during treatment)▪ Blood Dyscaria▪ ↑↑ Risk of agranulocytosismust monitor for this!INTERACTIONS ▪ Tobacco smoking—increases clearance of clozapine; dose may need to be adjusted if patient starts or stops smoking (the dose may need to be adjusted by 50%).▪ Avoid combinations with drugs that may cause agranulocytosis▪ GI obstruction may be exacerbated by the anticholiergic propertiesPATIENT COUNSELLING ▪ Need regular blood tests and other checks to monitor for serious side effects.▪ Do not stop taking this medicine suddenly unless your doctor tells you to.▪ Dose may need changing if you vary your caffeine intake (eg tea, coffee, coladrinks) or if you start or stop smoking tobacco; tell your doctor if any of these habits change.MONITORING ▪ Start treatment only if white cell count and absolute neutrophil count are normal; blood monitoring is required each week for the first 18 weeks and then each month▪ Medical supervision and resuscitation facilities must be available when treatment starts because of possible profound orthostatic hypotension with respiratory or cardiac failure▪ Monitoring for the development of myocarditis:- Baseline troponin + CRP + ECG + ECHO- Monitor CRP + TnI weekly for first 4 weeks- Enquire of symptoms every alternate day (when in patient)and weekly when out patient- Discontinuation of clozapine and investigation byechocardiography is advised if either troponin is in excess of twice the normal maximum or CRP is more than 100 mg/L. - Clinical – flu like illness, sudden BP drop, chest pain, non-specific ECG changes, basal crepitation’s, S3 heart sound, peripheral oedema, ↑ JVP</p>

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39
Q

<p>Factors contributing to antipsychotic medication adherence </p>

A

<p>PATIENT FACTORS ▪ Insight into their own condition▪ Attitude towards taking themedications▪ Medication beliefs (e.g. delusional beliefs the drug is poison)▪ Ongoing substance abuse▪ Psychotic symptoms (a psychotic person won’t remember to take their meds!)MEDICATION FACTORS▪ Side effects --> weight gain, motor symptoms, sedation, hyper- prolactinemia▪ Daily tablet dosing --> easy to miss or forget▪ Depo --> factors affecting access and adherence for repetitive doses▪ Efficacy▪ Time taken to show effect</p>

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40
Q

<p>Explain Antipsychotic medications to parent/ carer </p>

A

<p>▪ INDICATION + MECHANISM- to alleviate the positive symptoms of schizophrenia / psychosis. These include the hallucinations and delusions.- Work to reduce the effects of the chemicals in the brain that are causing the psychotic symptoms▪ OPTIONS- Consider whether a regular injection may suit you better than takingtablets.- This maybe an option that can’t be started off with but can be usedonce doses etc are titrated.▪ TAKING THE MEDS- It is best to avoid using illicit substances as use of cannabis or amphetamine markedly decreases control of psychotic symptoms and increases risk of relapse.- Taking your antipsychotic medicine regularly is important- Stopping or taking it irregularly is associated with high risk of relapse and suicide▪ SIDE EFFECTS- Extrapyramidal side effects are and what you can do about them- Risk of tardive dyskinesia with long-term antipsychotic treatment.- Sedation / drowsiness (↑ effects of alcohol, cannabis or sleepingtablets) = Do not drive or operate machinery- Metabolic effects + weight gain- You may feel dizzy on standing when taking this medicine. Get upgradually from sitting or lying to minimise this; sit or lie down if you become dizzy.▪ MONITORING + FOLLOW UP- Initially will need to check blood (UEC, LFT, prolactin) and ECG- Need annual / 6 monthly monitoring of metabolic variables and ECG- Prophylaxis is usually continued for 1–2 years after remission of a first psychotic episode (to prevent relapse) and for longer after >2 episodes- After stabilisation, the long half-life usually allows the total daily oral dose to be given at night</p>

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41
Q

<p>Lithium Initiation, dose, Patient education, monitoring, interactions, precautions, Adverse effects, what to do in pregnancy (MOOD STABILISER)</p>

A

<p>BEFORE COMMENCING/ INITIATION CHECK: ▪ UEC + eGFR (+/- urinalysis) ▪ Calcium + PTH levels ▪ Thyroid function (can cause hypothyroidism) ▪ ECG (can cause QTc prolongation) ▪ FBC (can cause leucocytosis) ▪ Weight + BMI (can cause gain) DOSE - 125 to 500 mg orally, BD daily for 2 weeks. Dose should then be adjusted according to the serum concentration determined after 5 to 7 days of steady-dose treatment. - Therapeutic range = 0.6 – 0.8mmol/L</p>

<p></p>

<p>PATIENT EDUCATION - Adherence is very very important! - Regular blood tests are important during treatment. - Take with food. - Do not break, crush or chew, and avoid taking with hot drinks. - Maintain a normal diet with regular salt and fluid intake. - Drink more non-alcoholic fluid during hot weather to avoid toxicity. - Avoid sodium bicarbonate (found in products such as indigestion medicines) as it makes lithium less effective. - Educate about lithium toxicity = Be alert for signs (eg extreme thirst and frequent urination, nausea and vomiting), esp during illness, excessive sweating or low fluid intake = If these occur, stop taking the tablets and seek medical attention immediately. - Abrupt cessation leads to relapse of mania within a few months, thus it should be withdrawn slowly over at least 2 months</p>

<p></p>

<p>MONITORING ▪ Measure serum levels 8 – 12 hours after last dose ▪ Serum [lithium] to be reassessed every 3 – 6 months once stable therapeutic concentration is achieved ▪ UEC+eGFRevery3–6months ▪ Thyroid function every 6 – 12 months ▪ Serum [calcium] annually (if ↑, measure PTH) Note: Monitor lithium concentration more frequently during illness (eg gastroenteritis), manic or depressive phases, changes in diet or temperature, pregnancy and concomitant medication (eg diuretics)</p>

<p></p>

<p>INTERACTIONS ↓ lithium renal clearance = [serum] ▪ Diuretics ▪ NSAIDs ▪ ACEi or ERBs ▪ Dehydration or intercurrent illness PRECAUTIONS ▪ Lithium is renally excreted --> ↓ dose in times of renal impairment ▪ Lower dose used in elderly (as they have worse kidney fn) ▪ Hyponatraemia increases the risk of lithium toxicity. Avoid lithium or use it cautiously where sodium levels may decrease (e.g. vomiting, diarrhoea, use of diuretics, dehydration, Addison’s disease). ▪ Psoriasis may be exacerbated or precipitated by lithium.</p>

<p></p>

<p>ADVERSE EFFECTS L - Leukocytosis I - Insipidus --> polyuria, polydipsia, decreased GFR, ESKD T - Tremors + ataxia H - Hypothyroidism I - Increased weight U - Underactive mind (dullness, fatigue, lethargy) M - Mothers --> teratogenic (esp T1 = Ebstein’s anomaly) GIT = nausea, vomiting, diarrhoea ECG = Long QTc, flat T waves, premature beats, conduction delays PREGNANCY ▪ If possible, avoid use particularly during the first trimester (TERATOGEN) ▪ However, at times keeping Lithium is the best option (as carbamazepine, valproate and lamotrigine are not suitable alternatives in pregnancy) ▪ More regular monitoring (every month) ▪ Monitor hydration ▪ Essentially a specialist’s job to deal with it + sort shiz out</p>

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42
Q

<p>Lithium toxicity - features, Acute vs. chronic, risk factors, key investigations, management</p>

A

<p>FEATURES<br></br>Early/mild= Nausea, vomiting, Tremor, Agitation, Proximal weakness, Poor memory, Flu-like illness<br></br>Moderate= Blurred vision, ↑ diarrhoea, N + V ▪ Muscle weakness, Drowsiness + apathy,Ataxia, Hypotension, ECG changes<br></br>Severe=Hypertonia, Hyperreflexia, Myoclonic jerks, Coarse tremor , Dysarthria, Disorientation, Psychosis, stupor, Seizures, Severe Hypotension, Coma<br></br>ACUTE TOXICITY= Rapid elimination by the kidneys and slow uptake into the CNS after overdose. Here, serum [ ] DOES NOT correlate to toxicity<br></br>CHRONIC TOXICITY= In patients taking therapeutic doses where there has been a change in dose, addition of other medications or decreased elimination (↓GFR). Here serum [ ] reflect CNS [ ] and they can be used to guide need for dialysis</p>

<p></p>

<p>RISK FACTORS ▪ Impaired kidney function ▪ Dehydration ▪ > 50 years ▪ Drug interactions or med changes ▪ Nephrogenic diabetes insipidus ▪ Thyroid dysfunction</p>

<p>KEY INVESTIGATIONS ▪ ECG ▪ FBC ▪ Serum lithium [ ] ▪ UEC ▪ eGFR</p>

<p>MANAGEMENT - Acute poisoning require no specific treatment except serial measurement of lithium concentrations to confirm elimination.<br></br>-Chronic poisoning has an insidious onset and more often requires treatment with intravenous fluids and occasionally dialysis.<br></br>-Clinical recovery can take days to weeks and is significantly delayed compared with the decrease in serum lithium concentrations.<br></br>-Some neurological effects may be permanent.<br></br>(1) Circulation ▪ Sufficient fluid replacement is essential ▪ IV Normal Saline is first line in those with normal renal function ▪ Patient may have DI, this must be taken into consideration when giving IV fluids (ie larger fluid requirements to replace increased urine output)</p>

<p>(2) Decontamination ▪ Decontamination is not indicated for acute ingestions < 50 g ▪ Activated charcoal does not bind lithium ▪ If ingested >50g, whole bowel irrigation can be considered if given within the first 6 hours and the patient is awake and cooperative<br></br>(3) Enhance elimination ▪ Should be discussed with a clinical toxicologist ▪ Haemodialysis increases the clearance of lithium, but is rarely required in patients with normal kidney function. ▪ Dialysis should be continued until lithium concentrations are below 1 mmol/L and further concentrations should be measured to detect rebound (4) Monitor lithium levels - Every 2 - 4 hours</p>

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43
Q

<p>LAMOTRIGINE - MOA, Indication, patient education, monitoring, adverse effects (MOOD STABILISER) </p>

A

<p>MOA Stabilises presynaptic neuronal membranes by blocking voltage-dependent and use- dependent sodium channels and inhibiting glutamate release.INDICATIONS - Epilepsy, bipolar mood stabilisation PATIENT EDUCATION▪ Tablets may be swallowed whole, chewed or dispersed in water.▪ This medicine may cause drowsiness, dizziness or blurred vision; if affected, do not driveor operate machinery.▪ Lamotrigine may also increase the effects of alcohol.▪ Tell your doctor immediately if you develop a rash, fever or swollen glands.▪ Stop treatment immediately if skin reaction or signs of hypersensitivity occur (with orwithout rash)MONITORING Before starting▪ FBC▪ UEC + eGFR▪ LFTOngoing Monitoring▪ FBC every 3 – 6 monthsADVERSE EFFECTS Common - diplopia, blurred vision- dizziness- ataxia- headache- somnolence- hyperkinesia- maculopapular rashUncommon- Alopecia- Severe skin reaction (TEN, SJS) - Multiorgan hypersensitivity syndrome - Aseptic meningitis - Low NE, low platelets Extra notes- Hepatically excreted --> avoid use in hepatic impairment - Teratogenic = patient must be on contraception </p>

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44
Q

<p>SODIUM VALPROATE - MOA, DOSE, INDICATION, PATIENT EDUCATION, MONITORING, ADVERSE EFFECTS (MOOD STABILISERS)</p>

A

<p>MOA - Multiple mechanisms. Prevents repetitive neuronal discharge by blocking voltage‐ and use-dependent sodium channels. Other actions include enhancement of GABA, inhibition of glutamate and blockade of T-type calcium channels.DOSE - 200 to 400 mg PO, BD. The dose should be ↑ weekly in increments of 200 to 400 mg/day and the serum concentration determined after 3 days of steady-dose treatment. - Most patients require a daily dose of 1500 to 3000 mg (1.5g – 3g)INDICATIONS - epilepsy, bipolar mood stabilisation, resistant migraines PATIENT EDUCATION ▪ Take with food to reduce stomach upset. Do not crush or chew tablets.▪ Valproate may make you feel drowsy; if affected, do not drive or operatemachinery. Valproate may also increase effects of alcohol.▪ Your appetite may increase when taking this medicine and you may need to pay more attention to your diet to avoid weight gain.▪ Tell your doctor immediately if symptoms such as fever, rash, abdominal pain,vomiting, jaundice, bruising or bleeding develop.▪ Do not stop taking this medicine suddenly unless your doctor tells you to.MONITORING Before starting▪ FBC▪ UEC + eGFR▪ LFTOngoing Monitoring▪ FBC every 3 – 6 monthsADVERSE V - VA - Appetite increase = wt gainL - Liver toxicityP - PancreatitisR - Reversible hair loss O - OedemaA - Ataxia, tremorT - Teratogen (NTD, congenital anomalies)E - Encephalopathy (from increased ammonia)NOTE Valproate reduces BMD and may increase fracture risk; consider BMD monitoring during long-term treatment and ensure vitamin D status and calcium intake are adequate</p>

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45
Q

<p>Valproate OD - Dose required to overdose, Features and management </p>

A

<p>Dose require to OD < 400mg/kg=little to no effect >400mg/kg = severe toxicity >1g/kg= life threateningFEATURES GIT = nausea, vomit, abdo painCNS = drowsy, ataxia, cerebral oedema, seizures, comaCV = long QTc, ↓ BP, ↑ HRMET = ↑Na, acidosis, ↑ LDH, ↓ Ca, ↓ BGL, ↑ ammoniaFBC =↓plt, ↓ NeMANAGEMENT Measure = ECG, [valproate], BGL, UEC, FBCAirway = severe may need support Circulation = IV saline resus, if severe give IV adrenaline Decontamination = activated charcoal within 2hHaemodialysis at specialist’s discretion</p>

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46
Q

<p>CARBMAZEPINE - MOA, INDICATIONS, PRECAUTIONS, PATIENT EDUCATION, MONITORING, ADVERSE EFFECTS (MOOD STABILISER) </p>

A

<p>MOA - Prevents repetitive neuronal discharges by blocking voltage-dependent and use- dependent sodium channels.INDICATIONS Epilepsy, Bipolar mood stabilisation, trigeminal neuralgiaPRECAUTIONS - Do not use in BM suppression, with clozapine or hypersensitivity history, hepatic ally excreted avoid use in hepatic impairment, teratogenic all female patients must be on contraception PATIENT EDUCATION ▪ Take with food to help prevent stomach upset. Do not chew or crush tablets▪ May cause drowsiness, dizziness or blurred vision especially at the start of treatment or whenthe dose is increased; if affected, do not drive or operate machinery.▪ May increase the effects of alcohol.▪ Interacts with grapefruit juice and many other drugs; avoid grapefruit juice and tell your doctorand pharmacist that you are taking carbamazepine before starting any new medication▪ Tell your doctor immediately if rash, sore throat, fever, mouth ulcers, bruising or bleeding occur.▪ Do not stop taking this medicine suddenly unless your doctor tells you to.MONITORING Before starting - FBC- UEC + eGFR- LFT Ongoing Monitoring - FBC every 3 - 6 months (BM suppression) - Monitor skin reactions - Consider BMD monitoring and vitamin D and calcium supplements ADVERSE C - ConfusionA -Ataxia R - Rash/ SJS / TEN T - Teratogen (contraception!!) D - DizzyD - Diplopia, blurred visionD - Drowsy H - Hypernatremia H - H reduced WCC H - Hepatotoxic </p>

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47
Q

<p>Anticonvulsant Hypersensitivity Syndrome - Onset, symptoms, management </p>

A

<p>ONSET - 1 – 4 weeks after starting therapySYMPTOMS - fever, rash and systemic organ involvement (lymphadenopathy, hepatitis,myositis, myocarditis, pneumonitis)- skin involvement (rash, SJS, TEN)- may affect the liver, kidneys and lungs and can lead to hepatic or renal failureMANAGEMENT - Stop offending drug, resus, rehydration, analgesia, burnsdressings, corticosteroids, ABx if infection suspected, consider plasma exchange </p>

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48
Q

<p>SSRIs - Examples, MOA, clinical pearls, side effects, risks </p>

A

<p>Examples - fluoxetine, citalopram, Escitalopram, Fluvoxamine Paroxetine SertralineMOA - selectively inhibit the presynaptic serotonin reuptake transporter --> ↑ 5HT in synapse↑ 5HT transmission in the brain- ↑ stimulation of 5HT receptors ↑ BDNF (↑gene transcription) BDNF increases neurogenesis in hippocampus and increases development of dendritic processes --> neuroplasticity too!Clinical Pearls- First Line + effective - Well tolerated in most people - Safe in OD- Can be used in pregnancy and breastfeeding (? Some PTL)- taken in the morning to minimise insomnia- Caution of increased suicidal thoughts and behaviour can occur soon after startingSE/RISKS- COMMON = nausea, diarrhoea, insomnia, drowsy, tremor, dry mouth, dizzy, sexual dysfunction, myalgia, rash- UNCOMMON = EPS, sedation, confusion, palpitations, ↓BP, ↑ bleeding re: ↓ plt function- SERIOUS = hepatitis, ↑ prolactin, akathisia, acute glaucoma- GI bleeding (caution if >80y, past UGI bleed or on NSAIDs) – by blocking 5HT uptake into platelets- Hyponatremia (esp in elderly)- Monotherapy in BPAD can precipitate mania- ↓ Dose in hepatic impairment- Serotonin syndrome (when combined with SNRI or MAOI) + QTc prolongation o Discontinuation syndrome (when stopping SSRI treatment taper over several weeks)</p>

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49
Q

<p>SNRI - Examples, MOA, Clinical pearls, SE/ RISKS </p>

A

<p>EXAMPLES- Duloxetine Venlafaxine DesvenlafaxineMOA- Inhibit serotonin and noradrenaline reuptake.- As they lack major receptor blocking actionsfewer side effects than TCAsClinical Pearls - Check BP before starting treatment, and then check regularly- Do UECs for [Na] at baseline, and then soon after starting treatment- Caution of increased suicidal thoughts and behaviour can occur soon after starting- You must taper dose if stoppingSE/ RISKS - COMMON = nausea, dry mouth, constipation, yawning, sweating, dizziness, increased BP, sexual dysfunction- UNCOMMON = orthostatic hypotension and fainting, palpitations, ↑HR o SERIOUS = seizures, akathisia, ↑ prolactin- GI bleeding (caution if >80y, past UGI bleed or on NSAIDs)- Hyponatremia (esp in elderly)- Monotherapy in BPAD can precipitate mania</p>

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50
Q

<p>TCAs - Examples, MOA, Clinical pears, SE/Risks </p>

A

<p>Examples - Amitriptyline Nortriptyline Imipramine ClomipramineMOA- Inhibit reuptake of NA+ 5HT into presynaptic terminals by binding to the amine transporter↑ NA + 5HT transmission- Unrelated to the therapeutic effects, TCAs also block cholinergic, histaminergic, alpha1-adrenergic and 5HT receptors.Clinical Pearls - Cheap- Effective in treating depression- Second line agents due to side effects and risk in ODMonitoring...- BP, FBC, LFT and ECG prior to starting- Assess suicidal ideation- Review in 2 – 3 weeks for effect + toleratingSE/ RISKS- Anticholinergic effects (hot, dry mouth, dry eyes, urine retention, blurred vision, constipation, confusion) – can’t see, cant pee, can’t spit, can’t shit- Cardiaco Arrhythmiaso Heart blocko Lengthen QTco Hypotension, reflex ↑HR- Sedation- Delirium (elderly)- Sexual (↓ libido, impotence)- Blood dyscarias, hepatitis- Precipitate acute angle glaucoma- Caution in hepatic impairment- DO NOT USE IN: prostatic hypertrophy, acute angle glaucoma, 2nd/3rd degree heart block o TOXIC IN OVERDOSE (suicide risk)</p>

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51
Q

<p>MAO-I - examples, MOA, Clinical pearls, SE/ Risks </p>

A

<p>Examples - Moclobemide Selegiline PhenelzineMOA- Inhibit monoamine oxidase A + B to thus ↓ break down of NA + 5HT + DA --> more NA + 5HT in synapses --> more transmissionClinical Pears - Third line agents in depression o Must avoid foods containing tyramine (aged cheese, salami) SE/ RISKS - COMMON = orthostatic ↓BP, insomnia, headache, drowsiness, agitation, tremors, twitching, hypereflexia, sexual dysfunction- UNCOMMON = itch, rash, sweating, blurred vision, peripheral oedema, hypoglycaemia - SERIOUS = Hypertensive crisis, hepatocellular damage- Contraindicated in = pheochromocytomas, use of sumatriptan, CVAs, Angina and epilepsy- Serotonin syndrome (when combined with SNRI or SSRI) - TOXIC IN OVERDOSE (suicide risk)</p>

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52
Q

<p>Mianserin Mirtazapine Trazodone - MOA, Clinical Pearls, SE/ RISKS</p>

A

<p>MOA - Mono-amine receptor antagonists that block various receptors to provide antidepressant effect.Clinical Pearls - Not used much- Not as effective as SSRIs, SNRIs or TCAsSE/ RISKS- Blocks histamine H1 receptors - > sedation- weight gain- fever + chills- memory problems</p>

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53
Q

<p>Benzo - diazepam 2-5mg, MOA, when/how to use, SE </p>

A

<p>MOA - Bind to y subunit of GABA receptor to potentiate its effect --> increased CL channel opening --> increased threshold --> decreased action potentials --> decreased NT release --> inhibitory effects and disinhibition - mainly in motor and limbic system When/how to use - Short term- Low dose- Regular schedule - Avoid PRN- Best in times of crisis (phobia, panic disorder, anxiety)Duration - 2 weeks - taper + cease by 6 weeks SE- Dependence- Withdrawal- Cognitive impairement - Falls Risk- Paradoxical aggression </p>

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54
Q

<p>Second generation antipsychotics adverse effects NOTE: see notes for specific SE of specific SGAs (table) </p>

A

<p>Common▪ Insomnia▪ Akathesia (very common!)▪ Headache▪ Sedation (esp Quetiapine and olanzapine)▪ Metabolic syndrome + weight gain▪ Cardiovascular- May increase the QT interval, increasing the risk of arrhythmia - orthostatic hypotension- some ↑ in VTE riskUncommon but Serious▪ Extrapyramidal Side effects - Dystonia- Akathesia- Pseudo-parkinsonism -Tardive Dyskinesia▪ Neuroleptic malignant syndrome (FARM symptoms)▪ Blood dyscrasias- anaemia, thrombocytopenia, neutropenia, agranulocytosis▪ New-onset or worsening obsessive-compulsive symptoms (clozapine)EXTRAPYRAMIDAL SIDE EFFECTS▪ highest with haloperidol, fluphenazine and trifluoperazine▪ lower with chlorpromazine, periciazine▪ Is dose dependant – so Reduce antipsychotic dose to avoid recurrent EPSENOTE: AKATHESIA= inner restlessness and a compelling need to be in constant motion, as well as by actions such as rocking while standing or sitting, lifting the feet as if marching on the spot, and crossing and uncrossing the legs while sitting</p>

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55
Q

<p>Clozapine - Indications, contraindications, receptor profile/MOA, adverse effects, interactions, patient counselling, monitoring (Antipsychotic) </p>

A

<p>INDICATIONS▪ Schizophrenia in people unresponsive to, or intolerant of, other antipsychotics (ie lack of satisfactory clinical response, despite the use of adequate doses of drugs from at least 2 groups of antipsychotics for a reasonable duration; or development of EPSE, including tardive dyskinesia)CONTRAINDICATIONS▪ Contraindicated in bone marrow disorders, drug-induced (including clozapine-induced) neutropenia or agranulocytosis (Neutropenia seems to be more common in children and adolescents than adults)▪ Severe Renal or Liver impairmentRECEPTOR PROFILE/ MOA▪ BLOCK 5HT2 to 90%▪ BLOCK D2▪ BLOCK M1▪ BLOCK D4(with high affinity related to plasma concentration)▪ BLOCK H1, alpha 1ADVERSE Common - Sedation ++- Hypersalivation ++ - Increase HR ++ - Constipation- Seizures - Pyrexia - Urinary incontinence Infrequent - Hepatitis ++- Myocarditis ++- Neutropenia ++- Angranulocytosis ++ - EPS ++- Eosinophilia - Priapism Rare - Cardiomyopathy ++- HTN- Myoclonic jerks - Interstitial nephritis - Fulminant hepatic necrosis Metabolic ▪ ↑↑ BGL. ↑↑ Lipids, ↑↑ weight▪ ↑↑ Risk of developing T2DM (must assess before + during treatment)▪ Blood Dyscaria▪ ↑↑ Risk of agranulocytosismust monitor for this!INTERACTIONS ▪ Tobacco smoking—increases clearance of clozapine; dose may need to be adjusted if patient starts or stops smoking (the dose may need to be adjusted by 50%).▪ Avoid combinations with drugs that may cause agranulocytosis▪ GI obstruction may be exacerbated by the anticholiergic propertiesPATIENT COUNSELLING ▪ Need regular blood tests and other checks to monitor for serious side effects.▪ Do not stop taking this medicine suddenly unless your doctor tells you to.▪ Dose may need changing if you vary your caffeine intake (eg tea, coffee, coladrinks) or if you start or stop smoking tobacco; tell your doctor if any of these habits change.MONITORING ▪ Start treatment only if white cell count and absolute neutrophil count are normal; blood monitoring is required each week for the first 18 weeks and then each month▪ Medical supervision and resuscitation facilities must be available when treatment starts because of possible profound orthostatic hypotension with respiratory or cardiac failure▪ Monitoring for the development of myocarditis:- Baseline troponin + CRP + ECG + ECHO- Monitor CRP + TnI weekly for first 4 weeks- Enquire of symptoms every alternate day (when in patient)and weekly when out patient- Discontinuation of clozapine and investigation byechocardiography is advised if either troponin is in excess of twice the normal maximum or CRP is more than 100 mg/L. - Clinical – flu like illness, sudden BP drop, chest pain, non-specific ECG changes, basal crepitation’s, S3 heart sound, peripheral oedema, ↑ JVP</p>

56
Q

<p>Anticonvulsant Hypersensitivity Syndrome - Onset, symptoms, management</p>

A

<p>ONSET - 1 – 4 weeks after starting therapy</p>

<p>SYMPTOMS - fever, rash and systemic organ involvement (lymphadenopathy, hepatitis, myositis, myocarditis, pneumonitis) - skin involvement (rash, SJS, TEN) - may affect the liver, kidneys and lungs and can lead to hepatic or renal failure</p>

<p>MANAGEMENT - Stop offending drug, resus, rehydration, analgesia, burns dressings, corticosteroids, ABx if infection suspected, consider plasma exchange</p>

57
Q

<p>SSRIs - Examples, MOA, clinical pearls, side effects, risks </p>

A

<p>Examples - fluoxetine, citalopram, Escitalopram, Fluvoxamine Paroxetine SertralineMOA - selectively inhibit the presynaptic serotonin reuptake transporter --> ↑ 5HT in synapse↑ 5HT transmission in the brain- ↑ stimulation of 5HT receptors ↑ BDNF (↑gene transcription) BDNF increases neurogenesis in hippocampus and increases development of dendritic processes --> neuroplasticity too!Clinical Pearls- First Line + effective - Well tolerated in most people - Safe in OD- Can be used in pregnancy and breastfeeding (? Some PTL)- taken in the morning to minimise insomnia- Caution of increased suicidal thoughts and behaviour can occur soon after startingSE/RISKS- COMMON = nausea, diarrhoea, insomnia, drowsy, tremor, dry mouth, dizzy, sexual dysfunction, myalgia, rash- UNCOMMON = EPS, sedation, confusion, palpitations, ↓BP, ↑ bleeding re: ↓ plt function- SERIOUS = hepatitis, ↑ prolactin, akathisia, acute glaucoma- GI bleeding (caution if >80y, past UGI bleed or on NSAIDs) – by blocking 5HT uptake into platelets- Hyponatremia (esp in elderly)- Monotherapy in BPAD can precipitate mania- ↓ Dose in hepatic impairment- Serotonin syndrome (when combined with SNRI or MAOI) + QTc prolongation o Discontinuation syndrome (when stopping SSRI treatment taper over several weeks)</p>

58
Q

<p>SNRI - Examples, MOA, Clinical pearls, SE/ RISKS </p>

A

<p>EXAMPLES- Duloxetine Venlafaxine DesvenlafaxineMOA- Inhibit serotonin and noradrenaline reuptake.- As they lack major receptor blocking actionsfewer side effects than TCAsClinical Pearls - Check BP before starting treatment, and then check regularly- Do UECs for [Na] at baseline, and then soon after starting treatment- Caution of increased suicidal thoughts and behaviour can occur soon after starting- You must taper dose if stoppingSE/ RISKS - COMMON = nausea, dry mouth, constipation, yawning, sweating, dizziness, increased BP, sexual dysfunction- UNCOMMON = orthostatic hypotension and fainting, palpitations, ↑HR o SERIOUS = seizures, akathisia, ↑ prolactin- GI bleeding (caution if >80y, past UGI bleed or on NSAIDs)- Hyponatremia (esp in elderly)- Monotherapy in BPAD can precipitate mania</p>

59
Q

<p>TCAs - Examples, MOA, Clinical pears, SE/Risks </p>

A

<p>Examples - Amitriptyline Nortriptyline Imipramine ClomipramineMOA- Inhibit reuptake of NA+ 5HT into presynaptic terminals by binding to the amine transporter↑ NA + 5HT transmission- Unrelated to the therapeutic effects, TCAs also block cholinergic, histaminergic, alpha1-adrenergic and 5HT receptors.Clinical Pearls - Cheap- Effective in treating depression- Second line agents due to side effects and risk in ODMonitoring...- BP, FBC, LFT and ECG prior to starting- Assess suicidal ideation- Review in 2 – 3 weeks for effect + toleratingSE/ RISKS- Anticholinergic effects (hot, dry mouth, dry eyes, urine retention, blurred vision, constipation, confusion) – can’t see, cant pee, can’t spit, can’t shit- Cardiaco Arrhythmiaso Heart blocko Lengthen QTco Hypotension, reflex ↑HR- Sedation- Delirium (elderly)- Sexual (↓ libido, impotence)- Blood dyscarias, hepatitis- Precipitate acute angle glaucoma- Caution in hepatic impairment- DO NOT USE IN: prostatic hypertrophy, acute angle glaucoma, 2nd/3rd degree heart block o TOXIC IN OVERDOSE (suicide risk)</p>

60
Q

<p>MAO-I - examples, MOA, Clinical pearls, SE/ Risks </p>

A

<p>Examples - Moclobemide Selegiline PhenelzineMOA- Inhibit monoamine oxidase A + B to thus ↓ break down of NA + 5HT + DA --> more NA + 5HT in synapses --> more transmissionClinical Pears - Third line agents in depression o Must avoid foods containing tyramine (aged cheese, salami) SE/ RISKS - COMMON = orthostatic ↓BP, insomnia, headache, drowsiness, agitation, tremors, twitching, hypereflexia, sexual dysfunction- UNCOMMON = itch, rash, sweating, blurred vision, peripheral oedema, hypoglycaemia - SERIOUS = Hypertensive crisis, hepatocellular damage- Contraindicated in = pheochromocytomas, use of sumatriptan, CVAs, Angina and epilepsy- Serotonin syndrome (when combined with SNRI or SSRI) - TOXIC IN OVERDOSE (suicide risk)</p>

61
Q

<p>DSM-V Criteria for Schizophrenia </p>

A

<p>A = ≥2 of the following, present for a significant portion of time during a 1 mo period (less if successfully treated). At least one of these must be (1), (2), or (3)1. Delusions2. Hallucinations3. Disorganized speech (e.g. frequent derailment or incoherence)4. Grossly disorganized or catatonic behaviour5. Negative symptoms(i.e. diminished emotional expression or avolition)B = ↓ level of function: for a significant portion of time since onset.- One or more major areas affected (e.g. work, interpersonal relations, self-care) is markedly decreased- If childhood/adolescent onset, failure to achieve expected levelC = at least 6 mo of continuous signs of the disturbance. Must include at least 1 mo of symptoms that meet Criterion A (i.e. active-phase symptoms) and may include periods of prodromal or residual symptoms(the disturbance may manifest by only negative symptoms or by two or more Criterion A symptoms present in an attenuated form - e.g. odd beliefs, unusual perceptual experiences)D = Exclude schizoaffective disorder and depressive or bipolar disorder with psychotic featuresE = Exclude other causes: GMC, substances (e.g. drug of abuse, medication)F = If history of autism spectrum disorder or communication disorder of childhood onset, the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations are also present for at least 1 mo</p>

62
Q

<p>DSM-V Schizoaffective disorder</p>

A

<p>A – An uninterrupted period of illness where there is <strong>concurrent psychosis (criterion A of schizophrenia) and major mood episode. </strong><br></br>B - <strong>delusions or hallucinations for ≥ 2 weeks in the absence of a major mood episode during the lifetime duration of the illness </strong><br></br>C - major mood episode symptoms are present for the majority of the total duration of the active and residual periods of the illness<br></br>D - the disturbance is not attributable to the effects of a substance or another medical condition<br></br>note: difference between schizophrenia and schizoaffective disorder is that<strong> schizoaffective disorder has a prominent MOOD component </strong>(manic or depressed) as apposed to schizophrenia where mode symptoms may present but they are NOT prominent</p>

63
Q

<p>DSM-V criteria Brief Psychotic Episode</p>

A

<p>A psychotic illness that meets criteria A + D + E of schizophrenia BUT with a very short duration of symptoms (1day - <1m total) with eventual resolution to full pre-morbid functioning. If the symptoms extend past 1 month, it become schizophreniform disorder. Managed with secure environment, antipsychotics and anxiolytics. This condition is self-limiting and has a good prognosis. Most return to normal pre-morbid functioning within a month.</p>

64
Q

<p>DSM-V for Schizophreniform disorder</p>

A

<p>A psychotic illness that meets criteria A + D + E of schizophrenia BUT with a shorter duration of symptoms (1 -6m total). If the symptoms extend past 6 months, it become schizophrenia.Full rapid resolution of symptoms is associated with better prognosis. Can develop into schizophrenia. </p>

65
Q

<p>DSM-V for a Delusional disorder</p>

A

<p>A = The presence of one (or more) delusions with a duration of 1 mo or longerB = Criterion A for schizophrenia has never been metNote: hallucinations, if present, are not prominent and are related to the delusional themeC = Apart from the impact of the delusion(s) or its ramifications, functioning is not markedly impaired, and behaviour is not obviously bizarre or oddD = If manic or major depressive episodes have occurred, these have been brief relative to the duration of the delusional periodsE = The disturbance is not attributable to the physiological effects of a substance, another medical condition or mental disorder</p>

66
Q

<p>DSMV Depressive episode </p>

A

<p>A = ≥ 5 of the following have been present during the same 2 week period and represent a change from previous functioning: (one must be low mood or anhedonia)a. Depressed Mood most of the day, nearly every day as indicated by either subjective report (empty, sad, hopeless) or observationb. Markedly diminished Interest or pleasure in all, or almost all activities most of the day, nearly every dayc. Significant weight loss / gain (e.g., ≥ 5% of body weight in a month) or decrease or increase in Appetite nearly every dayd. Insomnia or hypersomnia nearly every day (Sleep)e. Psychomotor agitation or retardation nearly every dayf. Fatigue or loss of Energy nearly every dayg. Feelings of worthlessness or excessive or inappropriate Guilt nearly every dayh. Diminished ability to think or Concentrate or indecisiveness nearly every dayi. Recurrent thoughts of death (suicidal ideations +/- plan or suicide attempt)B = Symptoms cause clinically significant distress or impairment in social, occupational or other important areas of functioningC = Episode is not attributable to physiological effects of a substance or to another medical condition"MSIG E CAPS"</p>

67
Q

<p>DSMV Manic Episode </p>

A

<p>For Bipolar, one must meet the following criteria of a manic episode (at least 1 episode in lifetime)A = A distinct period of abnormally and persistently elevated, expansive or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week + present most of the day, nearly every dayB = During the period of mood disturbance and ↑ energy or activity, ≥3 of the following are present to a significant degree and represent a noticeable change from usual behavioura. Inflated self-esteem (Grandiosity)b. Decreased need for sleepc. More talkative than usual or pressure to keeptalkingd. Flight of ideas or subjective experience that thoughts are racinge. Distractibilityf. Increase in goal directed Activity or psychomotor agitationg. Excessive involvement in Activities that have a high potential for Painful consequencesC = The mood disturbance is sufficiently severe to cause marked impairment for social or occupational functioning or to necessitate hospitalisation to prevent harm to self or others, or there are psychotic featuresD = The episode is not attributable to physiological effects of a substance or to another medical condition</p>

68
Q

<p>DSM-V Hypomanic episode </p>

A

<p>▪ Same as above but not severe enough to cause marked impairment for social or occupational functioning▪ It is associated with an unequivocal change in functioning that is uncharacteristic of individual when not symptomatic▪ Disturbance in mood and the change in functioning are observable by others</p>

69
Q

<p>Bipolar subtype 1 </p>

A

<p>▪ 1 or more manic or mixed episodes have occurred▪ Commonly accompanied by at least 1 MDE (but not needed for diagnosis)▪ If the patient needs hospitalisation or has psychotic symptoms it’s BPAD I▪ Disorder may become apparent after a patient is given a course of antidepressantmonotherapy for their depressive symptoms.</p>

70
Q

<p>Bipolar subtype 2</p>

A

<p>▪ 1 or more hypomanic episodes (4 or more weeks) AND 1 or more major depressive episodes▪ BPAD II is often under diagnosed + under reported as the MDEs are long and there is poor recognition of hypomanic episodes</p>

71
Q

<p>Cyclothymia </p>

A

<p>▪ Alternating between hypomanic and mild/moderate depressive symptoms for at least 2 years (never without symptoms for more than 2 months)▪ These people have never reached criteria for an MDE, manic or hypomanic eps.▪ Patients are higher functioning but the symptoms still cause distress or impairmentin important areas of functioning.▪ Management is the same as BPAD I = mood stabiliser +/- psychotherapy, avoidantidepressant monotherapy, address substance use.</p>

72
Q

<p>Dysthymia </p>

A

<p>▪ Long standing depressed mood but does not fulfil criteria for recurrent depressive disorder. They feel tired + depressed and everything is an effort</p>

73
Q

<p>DSM V Adjustment Disorder - Criteria, Clinical Presentation and Management Plan</p>

A

<p>CRITERIA/ CLINICAL PRESENTATION(A) Development of emotional or behavioural symptoms in response to an identifiable stressor(s) occurring within 3 months of the onset of the stressor(B) These symptoms / behaviours are clinically significant as evidenced by either of the following:• Marked distress that is in excess of what would be expected from exposure to the stressor• Significant impairment to social/occupational/academic functioning (C) The stress-related disturbance does not meet criteria for another mental disorder nor is it an exacerbation of a pre-existing mental condition(D) The symptoms do not represent normal bereavement(E) Once the stressor (or its consequences) has terminated, the symptoms do not persist for more than an additional 6 monthsSPECIFIERSo With depressed mood, with anxiety, with mixed anxiety/depression, with conduct disturbance (e.g. reckless driving,), unspecifiedRISK FACTORS / Stressor types▪ An individual’s personality and vulnerability to stress play an important contributing role▪ SINGLE = termination of relationship, loss of a loved one, loss of job▪ MULTIPLE = marked business difficulties, marital problems▪ RECURRENT = seasonal business crisis▪ CONTINUOUS  living in a dangerous neighbourhood, new stoma, dialysis▪ DEVELOPMENTAL EVENTS = going to school, leaving parental home, getting married, becoming a parent, failing occupational goals, retirementMANAGEMENT PLAN/APPROACHNon-Pharmacological▪ Brief psychotherapy= Individual or group= Group good for those with specific medical conditions▪ Crisis intervention▪ Education + social supports▪ Refer to online + written resources Pharmacological▪ Short course of benzodiazepines for those with significant anxiety symptoms (low- dose, limited duration)</p>

74
Q

<p>DSM-V Acute Stress Disorder - Criteria, Clinical Presentation and Management Plan </p>

A

<p>CRITERIA(A) Exposure to actual or threatened death, serious injury or sexual violence in oneof the following ways: direct experience, witnessing, learning about events happened to a close friend / family member, repeated/extreme exposure to adverse details of traumatic events (e.g. first responders, police officers)(B) Have ≥9 of the following symptoms of any of these 5 categories:▪ Intrusion symptoms (dreams, flashbacks, distress, memories)▪ Negative Mood▪ Dissociative symptoms (dazed, time slowing, 3rd person, amnesia)▪ Avoidance symptoms (of the memory or of people)▪ Arousal symptoms (insomnia, irritability, hyper-vigilance etc.)(C) Duration is 3days – 1 month after trauma exposure. (symptoms usually begin immediately after trauma and persist for at least 3 days, or up to a month)(D) The disturbance causes clinically significant distress or impairment in social, occupational or academic functioning(E) Condition is not attributable to drugs, other mental health disorder or organic illness.MANAGEMENT PLAN/APPROACH-->Aim = manage distress and prevent PTSD Psychological First Aid▪ Ensuring person’s safety + support (provide medical care if needed)▪ Acknowledge the stress reaction▪ Provide information about event + resolution▪ Offer practical assistance▪ Assess suicide risk, risk to others + dependants▪ One off debriefing is NOT recommended as they can increase symptoms andare not effective in treating ASD or preventing PTSD.Psychology Inputs▪ Psychoeducation to understand ASD and encourage use of inherent strengths, support networks and positive judgement.▪ Understanding of adaptive mechanisms and developing coping mechanisms▪ Cognitive behavioural therapy (good to decrease symptoms and ways to deal withfuture events)▪ Fostering + enhancing the therapeutic alliance Pharmacotherapy in select situations (Senior Doctor Discretion)▪ SSRIs for intrusive thoughts or low mood▪ Benzodiazepines for anxiety + insomnia▪ Anticonvulsants or Beta blockers may be helpful in some symptom clusters but this isat the specialist’s discretion</p>

75
Q

<p>DSM V PTSD – Criteria, Clinical Presentation and Management Plan</p>

A

<p>CRITERIA A) EXPOSURE to actual or threatened death, serious injury or sexual violence in one of the following ways: direct experience, witnessing, learning about events happened to a close friend / family member, repeated/extreme exposure to adverse details of traumatic events (e.g. first responders, police officers)(B) Presence of ≥1 of the following INTRUSION SYMPTOMS associated with the traumatic event (has started after the event):o Involuntary / recurrent / intrusive memorieso Involuntary / recurrent / intrusive dreams (event or affect)o Dissociative sx / flashbacks feeling like event is reoccurringo Intense / prolonged psychological distress at internal or external stimulithat resemble the evento Intense / prolonged physiological distress at internal or external stimulithat resemble the event(C) Persistent AVOIDANCE OF STIMULI associated with the event, as evidencedby one or both of the following:o Avoids distressing memories / thoughts / feelings re: the evento Avoids external reminders (people, places, conversations, activities, objectsetc.) that arouse distressing memories / thoughts / feelings re: the event(D) NEGATIVE ALTERATIONS in conitions + mood associated with the event, asevidenced by ≥2 of the following:o Amnesia re: event or parts of the evento Negative beliefs or expectations about oneself, others, or the worldo Distorted cognitions about the cause or consequences of the event that leadthe individual to blame them self or otherso Negative emotional state (e.g. fear, horror, anger, guilt, or shame)o Markedly diminished interest or participation in significant activities o Feelings of detachment or estrangement from otherso Persistent inability to experience positive emotions(E) Marked alterations in AROUSAL + REACTIVITY associated with the event, as evidenced by ≥2 of the following:o Irritable behaviour and angry outbursts - typically verbal or physical aggressiono Reckless or self-destructive behaviour o Hypervigilanceo Exaggerated startle responseo Problems with concentrationo Sleep disturbance (e.g. difficulty falling or staying asleep or restless sleep)(F) DURATION symptoms last > 1 month (occur within 6mo of event)(G) Causes clinically significant distress or impairment(social/occupational/academic)(H) Condition is not attributable to drugs, other mental health disorder or organicillness.Men’s trauma is most commonly combat experience/physical assault; women’s trauma is usually physical or sexual assaultCOMPLICATIONS / ASSOCIATED ISSUES▪ Substance abuse▪ Relationship difficulties▪ Depression▪ Impaired social and occupational functioning▪ Personality disorders (esp. Borderline PD)MANAGEMENT PLAN/APPROACHPSYCHOTHERAPY▪ Ensure safety and stabilize: emotional regulation techniques (e.g. breathing, relaxation)▪ Once coping mechanisms established, can explore/mourn trauma - challenge dysfunctional beliefs, etc.▪ Reconnect and integrate - exposure therapy, etc. PHARMACOLOGICAL▪ SSRIs (e.g. paroxetine, sertraline)▪ Prazosin (for treating disturbing dreams and nightmares)▪ Benzodiazepines (for acute anxiety)▪ Adjunctive atypical antipsychotics (risperidone, olanzapine) EYE MOVEMENT DESENSITISATION + REPROCESSING (EMDR)▪ an experimental method of reprocessing memories of distressing events byrecounting them while using a form of dual attention stimulation such as eyemovements, bilateral sound, or bilateral tactile stimulation▪ Its use is controversial because of limited evidence</p>

76
Q

<p>DSM-V - Generalised Anxiety Disorder: Criteria, Treatment</p>

A

<p>CRITERIA / PRESENTATION (A) Excessive anxiety + worry (apprehensive expectation), for more days than not for 6 months re: a variety of activities / events (B) Difficult to control the worry (C) Associated with ≥ 3 of the C-FIRST symptoms (D) Clinically significant impairment of function (E) Condition is not attributable to drugs, other mental health disorder or organic illness.</p>

<p>TREATMENT - Similar to panic disorder</p>

<p></p>

<p>EXCLUDE ORGANIC ILLNESS = Thyroid ↑, caffeine, stimulants, alcohol withdrawal = Adjustment disorder with anxious mood = If older person, think depression ot dementia with anxious mood</p>

<p></p>

<p>- LIFESTYLE = ↓ caffeine = Good sleep hygiene = Avoid alcohol and other drugs (must explore this area as many patients self-medicate) - PSYCHOTHERAPY (first line!!) = psychoeducation = CBT = interoceptive exposure (eliciting panic attack symptoms and learning how to tolerate them with coping strategies) = Stress management = scheduling, problem focused counselling = Relaxation techniques -</p>

<p>MEDICATIONS (if therapy alone is not enough) = 1st line – SSRIs / SNRIs (paroxetine, escitalopram, sertraline, duloxetine, venlafaxine) = 2nd line – buspirone (TID), buproprion (caution stimulating SEs) = Don’t need high doses usually = Add Benzodiazepines if needed (short-term, low dose, regular schedule, long half-life, avoid prn usage) = DO NOT USE BETA-BLOCKERS NOTE: C-First Symptoms Concentration Fatigue Irritability Restless Sleep Disturbance Tension (muscle)</p>

77
Q

<p>PHOBIC DISORDERS - Key criteria</p>

A

<p>KEY CRITERIA<br></br>- Exposure to the stimulus provokes an immediate anxiety response (?even panic attack)<br></br>- Person recognises fear as excessive / unreasonable<br></br>- Situations are avoided or endured with great stress/ distress/ anxiety - Significant interference with daily routine,/occupational/social functioning. Patient has marked distress.</p>

78
Q

<p>SOCIAL ANXIETY DISORDER - Criteria</p>

A

<p>1. Marked + persistent (>6 months) fear of social or performance situations in which one is exposed to unfamiliar people or possible scrutiny of others. They fear that they will act in a way that may be humiliating or embarrassing</p>

<p>2. The phobic situation(s) is avoided or is endured with intense anxiety or distress. - E.g. public speaking, initiating / maintaining conversation, dating, eating in public</p>

<p>MX;</p>

<p>- Psychological – CBT, social skills training</p>

<p>- Medications – SSRI best (need for ~ 6 – 12 weeks)</p>

<p>- Control of hyperventilation + Deep breathing<br></br>- Cognitive strategies<br></br>- Propranolol to manage specific symptoms</p>

79
Q

<p>Agoraphobia - Definition, Criteria, management</p>

A

<p>The fear and avoidance of being in places or situations from which escape might be difficult or embarrassing, or in which help might not be available in the event of suddenly developing a symptom that could be incapacitating or embarrassing. Most people with agoraphobia develop this in response to panic attacks.</p>

<p>CRITERIA</p>

<p>(A) Marked fear / anxiety re: 2/5 --> Using public transport --> Being in open spaces --> Being in closed spaces --> Standing inline or being in a crowd --> Being outside home alone</p>

<p>(B) ear that person fears / avoids situations because of thoughts that escape may be difficult or help will be unavailable should panic symptoms arise</p>

<p>(C) Situations provoke anxiety<br></br>(D) Situations are actively avoided, need a companion or are endured (E) The fear is out of proportion<br></br>(F) The fear / anxiety / avoidance causes functional impairment or distress<br></br>(G) Exclude organic or other MH issue (esp. obsessions, perceived flaws in appearance, PTSD, separation anxiety, paranoia)</p>

<p></p>

<p>Management<br></br>- Manage panic attacks --> SSRI or venlafaxine</p>

<p>- Behavioural therapy with graduated in vivo exposure to overcome the phobic avoidance</p>

80
Q

<p>Panic Attack Criteria/ definition</p>

A

<p>DEFINITIONS / CRITERIA PANIC ATTACK = an abrupt surge of intense fear or discomfort that reaches a peak within minutes. During this time one experiences ≥4 of the following symptoms: Mnemonic – STUDENTS FEAR 3CS<br></br>Sweating Trembling Unsteady/ dizzy Depersonalisation/ derealisation Excess HR/ palpitation Nausea Tingling/parasthesia SOB<br></br>FEAR- of dying, losing control, of going crazy Chest pain Chills or heat Choking feeling<br></br>NOTE: A panic attack is NOT a DSM-V disorder as it can occur in the context of other conditions.</p>

81
Q

<p>PANIC DISORDER - Criteria, Exclusions, DDx, Management </p>

A

<p>Definition = have panic attacks that have no apparent trigger + experience ≥ 1 month of anxiety about the panic attacks (persistent concern, anticipation, avoidance or significant maladaptive change). This is a DSM-V disorder.Exclusions - not attributable to medications, substance use, organic illness or other mental health disorder.DDX o Amphetamine, cocaine o Alcohol withdrawalo Opioid withdrawalo Arrythmiao Hypoglycemiao Cushings/ steroids o Hyperthyroidism o PETREATMENT Lifestyle- Explain why panic symptoms arise- Offer support + stress management- Limit caffeine and stimulant drinks- Good sleep hygiene- Advise that 50% - 80% improve with treatment, but most people have a chroniccourse and will need help to deal with psychological stressorsPsychological- Relaxation techniques = Visualisation= Controlled breathing techniques, box breathing(help alleviate ↓PCO2 and the associated symptoms)= Progressive muscle relaxation- CBT = interoceptive exposure (eliciting panic attack symptoms and learning how totolerate them with coping strategies)- Cognitive restructuring = address beliefs re: panic attacksPharmacological- FIRST LINE: (if CBT alone is not sufficient)= SSRIs – Fluoxetine, citalopram, paroxetine, fluvoxamine, sertraline= SNRIs – venlafaxine= May have transient increase in anxiety in first days but this resolves= Key SEs – GIT, flushing, sexual dysfunction, drowsy, dry mouth,= 2nd Line (TCAs, MAOIs and some benzoes)- Rules of thumb= Start low, go slow, aim high= Explain symptoms to expect prior to initiation (prevent non-compliance due to SEs)= Usually need high doses + longer therapy than depression (e.g. 12 wks) to see effect= Keep medicated for 6m - 1 year to avoid relapse (the can try stopping)- If Benzodiazepines needed short-term (1m max), low dose, regular schedule, long half-life, avoid prn usage- Try to avoid bupropion or TCAs - stimulating effects (exacerbate anxious symptoms)</p>

82
Q

<p>OCD - Criteria, Management<br></br>-hx points to ask about</p>

A

<p>CRITERIA / PRESENTATION</p>

<p>(A) Has obsessions / compulsions or both *OBSESSIONS = Recurrent / persistent thoughts, impulses or urges that are intrusive and unwanted. They cause marked anxiety or distress = Person tries to ignore or supress the urge or neutralise them with another action (i.e. the compulsion)</p>

<p>*COMPLULSIONS = Repetitive stereotyped behaviours (e.g. hand washing, door closing) or mental acts (e.g. praying, repeating words) that the person feel driven to perform in response to an obsession or in accordance to rules that must be applied = The acts are aimed at reducing the or preventing anxiety and distress from the situation.</p>

<p>(B) The obsessions / compulsions are time consuming (>1hr / day) or cause clinically significant distress and impairment of functionality (C) Condition is not attributable to drugs, other mental health disorder or organic illness.</p>

<p></p>

<p>MANAGEMENT</p>

<p>PSYCHOTHERAPY<br></br>- Cognitive Behavioural Therapy = Exposure with response prevention (exposure to fear situations with addition of how to prevent and challenge underlying beliefs)</p>

<p>MEDICATIONS</p>

<p>- SSRIs / SNRIs = need high dose + long duration – 12 – 18 week trials = if the condition improves and becomes stable, the medications can be reduces slowly and then stopped = they are best managed by a psychiatrist</p>

<p></p>

<p>Hx;<br></br>Obsessions - do you have troubling thoughts that keep bothering you and don't go away?</p>

<p>Compulsions - do you have to do certain things repeatedly even though you don’t want to?</p>

<p>Explore common - do you have do you check things a lot? Do you wash or clean a lot?, Are you concerned about putting things in special order?</p>

<p>Other screen - anxiety, depression</p>

<p>Function - do these activities interfere with your life and function?</p>

<p>Risk assessment</p>

<p>Precipitating &amp; perpetuating</p>

83
Q

<p>Cluster A - Weird/ MAD = general decryption of category</p>

A

<p>o Patients are odd / eccentric / withdrawn</p>

<p>o Familial Association (family Hx) with PSYCHOTIC DISORDERS o Higher risk of developing schizophrenia</p>

<p>o Defence mechanisms = intellectualisation + projection + magical thinking</p>

84
Q

<p>Paranoid Personality Disorder Criteria Parenting Defense</p>

A

<p>Pervasive distrust and suspiciousness of others; interpret motives as malevolent, beginning by early adulthood and presenting in variety of contexts with ≥4 Sx (SUSPECT)</p>

<p>S- Spousal infedility suspected U- Unforgiving (bears grudges) S- Suspect others of exploiting/decieving them P - Percieves attacks on character (+reacts quickly) E - Enemy or friend? (preoccupied with trustworthiness) C- Confiding in others is feared T - Threats interpreted in benign remarks/events Parenting - Harsh + punitive Defence Mechanism - Projection - Identification with the aggressor - Repression - Denial</p>

85
Q

<p>SCHIZOID Personality Disorder - Criteria, parenting, defence mechanisms</p>

A

<p>Pervasive pattern of detachment from social relationships (prefers to be alone + social withdrawal) and restricted range of emotions in interpersonal settings (eccentric + reclusive + restricted affect).</p>

<p>≥4 Sx (DISTANT)<br></br>D = Detached / flat affect (emotionally cold)<br></br>I = Indifferent to praise or criticism<br></br>S = Sexual experiences are of little interest<br></br>T = Tasks done alone<br></br>A = Absence of close friend<br></br>N = Neither desires nor enjoys close relationships<br></br>T = Takes pleasure in few / no activities<br></br>Parenting - Cold - Emotionally neglect<br></br>Defence mechanisms - Splitting - Projection - Denial - Rationalisation</p>

86
Q

<p>Schizotypal PD</p>

A

<p>Pervasive pattern of social and interpersonal deficits marked by acute discomfort with, and reduced capacity for, close relationships as well as by cognitive/perceptual distortions and eccentricities of behaviour. ≥5 symptoms (ME PECULIAR)<br></br>M - Magical thinking (superstitious)<br></br>E - Experiences unusual perceptions (e.g illusions)<br></br>P- Paranoid ideation<br></br>E - Eccentric behaviour/ appearance<br></br>C - constricted/ inappropriate affect<br></br>U - unusual thinking or speech<br></br>L - lacks close friends<br></br>I - ideas of reference (exclude delusions of reference)<br></br>A - Anxiety in social situations<br></br>R - Rule out psychotic or pervasive developmental disorders (not part of the A criteria)<br></br>Defence Mechanism - Denial - Projection - Acting out - Fantasy</p>

87
Q

<p>Cluster B - Wild/ Bad - general description </p>

A

<p>- Patients are dramatic, emotional and inconsistent- Familial association with MOOD DISORDERS- Defence mechanisms = denial, “acting out”, projection, idealisation / devaluation, regression (HPD), splitting (BPD)</p>

88
Q

<p>BORDERLINE PERSONALITY DISORDER - Criteria, parenting, defence mechanisms</p>

A

<p>Pervasive pattern of instability of interpersonal relationships, self-image and affects, and marked impulsivity. Has ≥5 symptoms (IMPULSIVE) I - impulsive (min 2. self damaging ways - sex, drugs, spending, driving) M - mood / affect instability P - paranoia / disassociation under stress U - unstable self image L - labile + intense relationship S - suicidal gestures/ self harm I - inappropriate anger V- vulnerable to feeling abandoned (real or imagine --> frantically) E = Emptiness (feeling of) Parenting - Severe developmental trauma - sexual abuse - significant emotional abuse/ neglect Defence - Dissociation - Splitting - Projection </p>

89
Q

<p>Antisocial Personality Disorder - Criteria, parenting, defence </p>

A

<p>Pervasive pattern of disregard for and violation of rights of others in a person > 18years old. Features occured since 15yo (+had conduct disorder when they were <15yo). ≥5 symptoms: (CORRUPT)C - cannot confirm to law, moral values or societal norm (repeatedly offend) O - obligations ignored (irresponsible, can't honour work behaviour or financial obligations. Ignore/ don't care about their children) R - Reckless disregard for safety R - Remorseless U - Underhanded (deceitful, lie, ise aliases) - lie a lot, thus collateral history for diagnosis P - Planning insufficient (impulsive)T- Temper (irritable and aggressive - poor impulsive control) Parenting - Inconsistent parenting - Ineffectual or harsh discipline - Parental criminality and parental substance abuse Defence mechanism - Repression - Denial - Splitting </p>

90
Q

<p>Narcissistic Personality Disorder - Criteria, parenting, defines mechanisms </p>

A

<p>Pervasive pattern of grandiosity (in fantasy or behaviour), need for admiration and lack of empathy. Has ≥5 symptoms: (GRANDIOSE)G - grandiose (exaggerates achievements + talents, undervalue others) R- Requires constant attention + admirationA- arrogant N - needs to be special (+associate with other specials/high-status people) D - dreams of success, power, beauty and love I- interpersonally exploitive (takes advantage of others for their own gain) O- others - lack empathy, recognising other's needsS- sense of entitlement E- envious (or believes others are envious) Parenting - emotional neglect- empathic failure- inability to form meaningful relationshipsDefence Mechanisms - Denial- Splitting - Projection- Intellectualisation - Rationalisation </p>

91
Q

<p>Histrionic Personality Disorder </p>

A

<p>Pervasive pattern of excessive emotionality and attention seeking. Dramatic, flamboyant, extroverted. Has ≥5 symptoms: (ACTRESSS)A - appearance used to attract others C- centre of attention always T- theatricalR- relationships (perceived more intimate than they are)E- easily influenced S- seductive/ provocative behaviour S- shallow expression of emotion (rapidly shifts)S - speech (impressionistic + vague) Parenting - Perceived rejection by same sex parent and identification with opposite sex parent often apparentDefence mechanism - Projecting- Splitting- Fantasy </p>

92
Q

<p>Cluster C - Worried/ Sad. General definition + treatment </p>

A

<p>- People are anxious and fearful Familial association with ANXIETY DISORDERS - Defence mechanisms = isolation, avoidance, hypochondriasisTreatmento Social skills trainingo Self-empowermento Anxiety managemento Group-therapy (safe social situations + build social skills)</p>

93
Q

<p>Avoidant Personality Disorder - criteria, parenting, defence mechanism </p>

A

<p>Pervasive pattern of social inhibition, feelings of inadequacy and hypersensitivity to negative evaluation. Fear embarrassing themselves in social situations – so isolate themselves. ≥4 symptoms: (CRINGES)C- criticism or rejection preoccupies thoughts in social situations R- Restraint in relationships due to fear of shame I- Inhibited in new relationships (fear of inadequacy) N- Need to be sure they're liked before engaging socially G- gets around occupational activities with need for interpersonal contact (e.g reject promotion as can get criticised in new role)E- Embarrassment prevents new activity/ risk taking S- self viewed as unappealing Parenting - Rejection- Severe life threatening/ disfiguring illnessDefence - Projection- Denial- AvoidanceNote: Fear social interaction but crave for it. Very sensitive to criticism</p>

94
Q

<p>Dependant Personality Disorder - Criteria, parenting, defence. </p>

A

<p>Pervasive and excessive need to be taken care of that leads to submissive and clinging behaviours and fears of separation. Difficulty making everyday decisions. ≥5 symptoms: (RELIANCE)R- Reassurance needed for everyday decisions E- Expressing disagreement difficult L- Lifestyle responsibilities assumed by others I- Initiating projects difficult (lack of confidence) A- Alone (feel helpless/ uncomfortable when alone)N- Nurturance (excessive lengths to obtain it)C- Companionship sought urgently when relationships end E- exaggerated fears of being left to care for self Parenting - Separation and losses (physical illness, chronic illness, parental chronic illness or death) Defence mechanisms - Denial - Repression </p>

95
Q

<p>Obsessive- compulsive PERSONALITY disorder - criteria, parenting, defence mechanisms </p>

A

<p>Pervasive pattern of preoccupation with orderliness, perfectionism and mental and interpersonal control at expense of flexibility, openness and efficiency. ≥4 symptoms: (SCRIMPER)S- stubbornC- cannot discard worthless objects R- rule/ detail obsessed (point of activity lost) I - inflexible re: mortality, ethics and valuesM- miserly (\$\$ is hoarded for future catastrophes) P- perfectionistic (?interfere with task completion)E- exclude leisure due to devotion to workR - Reluctant to delegates to others Parenting- Authoritarian and moralising, inducing shame and guilt Defence - Denial- Reaction formation- Intellectualisation- Isolation of affect </p>

96
Q

<p>Management of Borderline personality Disorder</p>

A

<p>CRISIS/ EMERGENCY<br></br>- When a BPD patient is at risk of suicide or serious self-harm<br></br>(1) MANAGE AFFECT STORM<br></br>o Project calmness and confidence<br></br>o Engage the patient in a dialogue<br></br>o Clarify emotions o Identify precursors and triggers<br></br>o Explore positive and negative solutions</p>

<p>(2) RISK ASSESSMENT<br></br>o Distinguish chronic risk from acute-on-chronic risk<br></br>o Assess suicide risk, homicide risk and substance abuse<br></br>o Dynamic factors: --> recent change in social network --> several recent acute life events --> change in drug/alcohol use --> recent hospital discharge --> high level of hopelessness</p>

<p>(3) MANAGE OWN COUNTER-TRANSFERENCE</p>

<p>(4) SHORT TERM ADMISSION IF NEEDED</p>

<p><br></br>Psychotherapy<br></br>TYPES ON OFFER<br></br>- Psychodynamic Psychotherapy<br></br>-Cognitive Behavioural Therapy -->Dialectical behavioural therapy or Schema-focused therapy</p>

<p></p>

<p>PHARMACOTHERAPY<br></br>- DO NOT USE medicines as main treatment for BPD, because medicines only make small improvements in some symptoms of BPD,<br></br>- Only consider meds in crisis situations (SSRI - fluoxamine , atypical antipsychotics or mood stabilisers)</p>

<p></p>

<p>CASE MANAGEMENT<br></br>-long term continuity, realistic goals, addressing secondary problems (substance abuse)</p>

97
Q

<p>Anorexia Nervosa DSMV criteria, severity, type, RF, clinical signs, IX, indications for admission, management</p>

A

<p>DSM<br></br>(A) RESTRICTION OF ENERGY INTAKE relative to requirements, leading to a significantly low body weight in the context of age, sex, development, and physical health.<br></br>(B) FEAR OR BEHAVIOUR: intense fear of gaining weight or of becoming fat, or persistent behaviour that interferes with weight gain. (C) PERCEPTION: disturbance ofbody weight or shape, persistent lack of recognition of the seriousness of the low body weight</p>

<p></p>

<p>Severity<br></br>- BMI >17 = mild<br></br>- BMI 16 - Moderate<br></br>- BMI <16 = severe<br></br>Type<br></br>- Restrictive = no binge/purging in last 3 months<br></br>- Purging = binge/purging in last 3 months</p>

<p></p>

<p>RF;<br></br>family history, exercise where height/weight are critical, anxiety, depression, OCD, borderline, low self esteem, abuse, substance disorder<br></br></p>

<p>Signs; extremely low body weight, obvious bony prominences, proximal muscle wasting,breast atrophy, amenorrhea, abdominal pain/constipation, lanugo, brittle hair/nails, dry skin, low BP/HR/RR/T</p>

<p><br></br>Ix; looking for complications--> ECG (long QT, hypokalemia), FBC (normocytic normochromic anaemia, leucopenia), UEC/CMP (refeeding syndrome- hyponatremia/kalemia/phosphatemia/magnesia), TFT (hypothyroidism), hyercholesteorlemia, high LFT (starvation hepatitis), BMD scan, low LH/FSH/, high cortisol</p>

<p></p>

<p>MANAGMENT Usually outpatient therapy.<br></br>Indications for admission;</p>

<p>-Weight - severely low BMI (<14) OR rapid weight loss despite intervention OR several days of no oral intake</p>

<p>-Cardiac - bradycardia <45, BP < 90/60, ECG abnormal (arrhythmia, prolonged QT)</p>

<p>-Hypothermia <36</p>

<p>-Electrolyte disturbance (e.g. hypokalemia, hypoglycaemia)</p>

<p>-Suicidal ideation</p>

<p>-Failed outpatient therapy<br></br></p>

<p>Majority is managed as outpatient;<br></br>Educate patient and family<br></br>Involve MDT (GP, pscyh, dietician, school counsellor)<br></br>Pscyhotherapy; CBT, family therapy, supervised weight gain therapy<br></br>Pharm; not usually used unless serious comorbidities--> antidepressants, bisphosphonates/vit D/calcium, other supplements (zinc, iron, folate, VB12)</p>

98
Q

<p>Bulimia Nervosa - Criteria, Management<br></br>-Complications</p>

A

<p>CRITERIA</p>

<p>(A) RECURRENT EPISODES OF BINGE EATING characterised by both of the following:<br></br>a. Eating, in a discrete period of time (e.g., within any 2 hour period), an amount of food that is definitely larger than what most individuals would eat in a similar period of time under similar circumstances<br></br>b. A sense of lack of control over eating during the episode<br></br>(B) RECURRENT INAPPROPRIATE COMPENSATORY BEHAVIOURS in order to prevent weight gain, such as self- induced vomiting, misuse of laxatives, diuretics,; or excessive exercise.<br></br>(C) The binge eating and inappropriate compensatory behaviours both occur, on average, AT LEAST ONCE A MONTH FOR 3 MONTHS<br></br>(D) Self-evaluation is unduly influenced by body shape and weight.<br></br>(E) The disturbance does not occur exclusively during episodes of AN.<br></br></p>

<p>MANAGEMENT<br></br>- Cognitive behavioural therapy<br></br>= Educate re: nutrition, shape + weight + complications<br></br>= self-monitoring of relevant thoughts and behaviours<br></br>= identify and challenge problematic thoughts etc.<br></br>- SSRI (fluoxetine 20mg OD) – may be related to a specific serotonin modulating effect on satiety mechanisms</p>

<p>Complications; sialedenitis, parotid gland enlargement/tenderness, russels sign, enamel erosion,esophagitis, upper GIT and esophageal tears (presents with haematemesis), perforations are extremely rare but life-threatening, Vomiting - hypochloremic metabolic alkalosis (vomiting), hypokalaemia, hyponatremia, Laxatives - normal anion gap metabolic acidosis,palpitations, arrhythmia (electrolyte imbalance)</p>

<p><br></br>Mx;<br></br>- Inpatient management only if: at risk of suicide, medically unwell, serious electrolyte anomalies, in the first trimester of pregnancy (spontaneous abortion risk)<br></br>-Same as anorexia; CBT and SSRI if indicated<br></br>Note: Hypokalaemia (and subsequent cardiac dysrhythmia) is an important complication of purging and/or self-induced vomiting; potassium replacement can be lifesaving – SO THINK OF CHECKING + TREATING!</p>

99
Q

<p>Binge Eating Disorder - Criteria, management</p>

A

<p>CRITERIA</p>

<p>(A) Recurrent episodes of binge eating (as in BN)</p>

<p>(B) The binge eating episodes are associated with three (or more) of the following:<br></br>a. Eating more rapidly than normal<br></br>b. Eating until feeling uncomfortably full<br></br>c. Eating large amounts of food when not feeling physically hungry<br></br>d. Eating alone because of feeling embarrassed by how much one is eating<br></br>e. Feeling disgusted with oneself, depressed, or very guilty afterwards<br></br><br></br>C) Marked distress regarding binge eating is present<br></br>(D) The binge eating occurs, on average, at least once a week for 3 months<br></br>(E) The binge eating is not associated with the recurrent use of inappropriate compensatory behaviour (i.e. exclude BN) and does not occur exclusively during<br></br><br></br>AN MANAGEMENT<br></br>- CBT or IPT<br></br>- Weight loss programs<br></br>- Dietician advice<br></br>- SSRIs may be useful as adjunct to psychotherapy</p>

100
Q

<p>Avoidant/ Restrictive Food intake disorder</p>

A

<p>DEFINITION<br></br>- Eating disturbance to the extent of persistent failure to meet appropriate nutritional and/or energy needs, resulting in significant weight loss/growth failure and nutritional deficiencies.<br></br>- Patients experience disturbances in psychosocial functioning and may become dependent on enteral feeding/ oral nutritional supplementation<br></br>- NO binges + purges i.e. not BN<br></br>- No evidence of distress in the way in which one’s body weight or shape is experienced i.e. not<br></br><br></br>AN MANAGEMENT<br></br>- Watch and wait<br></br>-Behavioural modification<br></br>- Psychotherapy</p>

101
Q

<p>What are the effects of each of the following pathways + what pathology can result from altered dopamine levels in these pathways;<br></br>-Mesolimbic<br></br>-Mesocortical<br></br>-Nigrostriatal<br></br>-Tuberoinfundibular</p>

A

<p>-Mesolimbic= emotions and reward--> if there is increase dopamine in this pathway it causes positive symptoms of schizophrenia (hallucinations and delusions)<br></br>-Mesocortical= cognition and executive function--> if there is decreased dopamine in this pathway it causes negative symptoms of schizophrenia (depression, psychomotor retardation)<br></br>-Nigrostriatal= movement (as involves the basal ganglia)--> low dopamine causes extrapyramidal side effects<br></br>-Tuberoinfundibular= prolactin regulation--> low dopamine causes increased prolactin</p>

102
Q

<p>Neuroleptic Malignant syndrome<br></br>-mechanism<br></br>-RF<br></br>-presentation<br></br>-management</p>

A

<p>-Massive dopamine blockade causing increased dopamine in the synaptic clefts--> caused by increased drug dosage/medical illness/dehydration/decreased nutrition--> most common in young men<br></br>-CAN BE FATAL<br></br>-FALTER symptoms;<br></br>F= fever<br></br>A=autonomic symptoms (tachycardia, tachypnea, hypertension, hyperthermia)<br></br>L=leucocytosis<br></br>T=transaminases<br></br>E= elevated enzymes (high CK), high potassium<br></br>R=rigidity</p>

<p>-can present over months/years</p>

<p>Mx;<br></br>-cease medication and consult psychiatrist<br></br>-symptomatic= fluids, cooling blankets, treat hyperkalemia, +/- mechanical ventilation, DVT prophylaxis<br></br>-can use alternative meds; anticholinergics or benzos for muscle rigidity, oral bromocriptine (DA antagonist), IV dantrolene (muscle relaxant)<br></br>-cease antipsychotic and</p>

103
Q

<p>Serotonin Syndrome<br></br>-how does it happen<br></br>-presentation<br></br>-management</p>

A

<p>-Due to sudden increase in serotonin (either through SSRI/MAO-I combination drugs or increased dose or introduction of antibiotics like linezolid that are similar structure to serotonin)<br></br><br></br>Cognitive; agitation, insominia, hallucinations, restlesness, euphoria, hypomania<br></br>Autonomic; tachycardia/pnea, hypertension, fevers, diaphoresis, mydriasis, arrhythmias<br></br>Neuromuscular; tremor, clonus, ataxia, incoordination, seizures, hyperreflexia</p>

<p>-Rapid onset of 6 hours but can take days to wear off</p>

<p><br></br>Mx;<br></br>1. cease antipsychotic<br></br>2. general supportive care; cooling blankets, volume replacement, rehydration, benzodiazepines<br></br>3. cyproheptadine as antidote</p>

104
Q

<p>ECT<br></br>-what is it<br></br>-indications<br></br>-contraindications<br></br>-adverse effects<br></br>-alternatives</p>

A

<p>-Psychiatric treatment where you are placed under GA then electricity is used to stimulate a minor controlled seizure --> this has been shown to be very effective for certain psychiatric disorders</p>

<p>-Indicated for; severe depression, bipolar or schizophrenia not responsive to treatment, catatonic depression, severe PND, strong suicidal ideation<br></br><br></br>CI; cardiac disease (CHF, IHD) or neurological disease (stroke, high ICP)<br></br><br></br>Adverse; muscle pain, confusion, short or long term memory loss, headache, N/V<br></br>-rare; stroke, not responsive to tx, prolonged seizure, MI, death</p>

<p></p>

<p>Before; fast for 6 hours, pre-ECG, cease lithium/benzos/antiepileptics, FBC, UEC, BGL, CXR<br></br>During; sedated with propofol+ketamine, shock waves delivered under anaesthetic observation<br></br>-watch for response and tailor level according to post-ictal EEG</p>

105
Q

<p>Clinical features that occur with stopping anti-depressants<br></br>-average time for antidepressants to become effective</p>

<p>-common side effects of antidepressants</p>

A

<p>-Flu-like symptoms, insomnia, nausea, postural imbalance, sensory disturbances, hyperarousal<br></br>-Medication should be tapered slowly and halfed each week until it is at its lowest dose and then it can be ceased<br></br><br></br>-become effective after 4-6 weeks<br></br>-side effects normally reduce after 1-2 weeks as tolerance builds</p>

<p></p>

<p>-bleeding, hyponatremia, sedation, dry mouth, constipation, orthostatic hypotension, sexual dysfunction, weight gain</p>

106
Q

<p>Psychosis<br></br>-definition<br></br>-4 cardinal features<br></br>-what disorders does psychosis occur in<br></br>-what organic diseases can present with features of psychosis</p>

A

<p>-Loss of contact w reality; unable to distinguish between real and false perception<br></br>-4 signs; hallucinations, delusions, disordered thinking (thought disorders) and disordered behaviours (aggression and agitation)<br></br>-Psychosis is seen in schizotypal PD, bipolar, drug induced psuchosis, psychotic depression, schizophrenia etc<br></br><br></br>-organic; thyroid disease, adrenal disease, wilsons disease, huntingtons disease, alzheimers disease</p>

107
Q

<p>A patient has 3 weeks of hallucinations, delusions and paranoia, followed by another 4 weeks of excessive spending, no sleep and sexual disinhibition whilst still remaining paranoid<br></br>They have;<br></br>MDD with psychosis<br></br>Bipolar with psychosis<br></br>Schizoaffective disorder; bipolar type<br></br>Schizoaffective disorder; depressive type</p>

A

<p>Schizoaffective disorder; bipolar type<br></br>-had schizophrenic symptoms first and then developemed manic symptoms after 3 weeks</p>

108
Q

<p>What is the defition of a;<br></br>-Brief psychotic disorder<br></br>-Schizophreniform disorder<br></br>-Schizophrenia<br></br>-Schizoid personality<br></br>-Schizotypal personality<br></br>-Delusional disorder</p>

A

<p>-Brief psychotic disorder= a psychotic illness that meets criteria A +D +E of schizophrenia (will have delusions/hallucinations, not attributed to schizoaffect disorder/MDD with psychosis) and not due to other substances or organic causes--> lasts less than 1 month, often due to stressors/post-partum, will have eventual resolution to pre-morbid functioning- manage with antipsychotics/anxiolytics</p>

<p><br></br>-Schizophreniform disorder=a psychotic illness that meets criteria A +D +E of schizophrenia (will have delusions/hallucinations, not attributed to schizoaffect disorder/MDD with psychosis) and not due to other substances or organic causes--> can develop into schizophrenia but good prognosis associted with acute onset/confusion/good pre-morbid condition, abscece of/blunted affect</p>

<p><br></br>-Schizophrenia= DSM V criteria lasting longer than 6 months<br></br><br></br>-Schizoid personality= personality type; DISTANT; detached/flat affect, indifferent to criticism/praise, sexual experiences of little interest, tasks done on solidarity, absence of close friends, neither desires or enjoys close relationships, takes pleasure in few activities (difficult to avoidant personality as avoidant wants a relationship but is scared of one)</p>

<p><br></br>-Schizotypal personality= ME PERCULIAR; magical thinking, experiences unsual perceptions, paranoid ideation, exxentric behaviour or appearance, constricted or innap affect, unusla thinking/speech, lacks close friends, ideas of reference, anxiety in social situations, rule out psychotic disorders</p>

<p></p>

<p>-Delisional disorder= presence of one or more delusions for a duration of 1 mo or longer, but not all components of criteria A for schizophrenia has been met, functioning is not impaired, only brief manic/depressive episodes have occurred, delusions are not attributed to a substance or another medical condition</p>

109
Q

<p>Differentials of a patient presenting with acute psychosis<br></br>History points to ask for a patient presenting with acute psychosis<br></br>What exams would you do for a patient with psychosis<br></br>IX for a pt with psychosis</p>

A

<p>DDX;<br></br><strong>Medical- </strong>neurological (dementia, delirium, head injury, brain tumour, stroke, CNS infection, intracranial bleed, seizures), endocrine (hypo/hyper thyroidism, parathyroidism, cushings disease, addisons disease), metabolic (electrolyte imbalance (BSL, Ca, Na, O2), organ failure (hepatic encephalopathy), B12/Folate deficiency<br></br><strong>Intoxication/withdrawal-</strong>illicit drugs (cocaine, LSD, meth), prescribed drugs (levodopa, anticholingergics, steroids, thyroxine), alcohol<br></br><strong>Psychotic disorder-</strong>brief psychotic episode, schizophreniform disorder, schizophrenia, schizoaffective disorder<br></br><strong>Mood disorder-</strong>depression with psychotic features, bipolar affective disorder<br></br><strong>Personality disorder-</strong>schizotypal, schizoid, BPD, paranoid PD</p>

<p></p>

<p>HX<br></br>-hx of recent head trauma<br></br>-recent seizures or hx of known seizure disorder<br></br>-signs of intracranial path- focal neurological symptoms, new onset headache, visual/speech changes, abnormal movements, memory loss<br></br>-fluctuating consciousness- delerium<br></br>-PMHX; thyroid, adrenal, organ failure (hepatic encephalopathy, uremia), multiple myeloma/other malignancy (brain mets), psychiatric conditions<br></br>-Medications/substances; alcohol, illicit drugs, prescriptions (opiods, steroids, thyroxine, levodopa), toxins (heavy metals, organophosphates)<br></br>-Diet- VB12/Folate deficiency<br></br>-Fam hx; neurological/medical, psychiatric<br></br>-Complete psych hx; premorbid functioning, developemental hx, collateral hx, risk assessment</p>

<p></p>

<p>Exam;<br></br>Vitals; infeciton, intoxication, withdrawal<br></br>Appearance; cachectic, dishevelled, confused<br></br>GCS/Orientation<br></br>Neuro exam; meningitis, encephalitis, focal deficits (brain lesions)<br></br>Thyroid/cushings exam; hyper/hypo features + cushing features (steroid induced psychosis)<br></br>Features of SLE; joint deformities, rash<br></br>MSE</p>

<p></p>

<p>Ix;<br></br>-FBC, UEC, GFR, CMP, TFT, LFT, VB12/Folate, ANA/ESR<br></br>-Urinalysis/MCS/Drug screen<br></br>-CXR (infeciton sites)<br></br>-Others; syphilis, blood cultures, troponins, ECG, coag<br></br>-Head imaging only indicated if cranial pathology is suspected or focal neural deficits present (head trauma, motor anomaly, hydrocephalus)</p>

110
Q

<p>What is the management of a patient who is acutely psychotic/disturbed (ED)</p>

A

<p>Behavioural/non-pharm approach;<br></br>-Calm, quiet environement, remove objects that could be weapons, keep a clear exit, have a non-threatening stance<br></br>-Consider admission to acute ward<br></br>-Keep carer/support person around</p>

<p></p>

<p>Medical;<br></br>-Oral benzo (lorazepam) +/- antipsychotic (olanzapine or haloperidol)<br></br>-May need to use IM if patient refuses oral<br></br>-repeat dosing every 45-60min</p>

111
Q

<p>What are the clinical features/phases of schizophrenia<br></br>-what is the prog<br></br>-what is the mx (medical and non-medical)</p>

A

<p>-Phases; premorbid, prodome, active (positive sx), remission (neg sx), relapse<br></br>-Positive sx; delusions, hallucinations, disorganised thoughts and behaviours<br></br>-Neg sx; depression, anhedonia, avolition, alogia</p>

<p></p>

<p>Good prognosis if; female, acute onset, good premorbid functioning, short duration of symptoms, no fam hx, no structural brain anomaly, good response to medications, good support system<br></br>-1/3rd improve, 1/3rd worsen, 1/3rd stay same</p>

<p><br></br>Mx;<br></br>-SGA; risperidone, olanzepine, quitiapine, apiprazole<br></br>-need to give with a benzodiazepine as SGA take around 2-4wks to work<br></br>-Review after 2-3 weeks, if symptoms still not controlled trial on a different SGA--> if still not controlled then put on clozapine<br></br>-Start with minimum dose of all SGAs--> if after first presentation remain on medication for at least one year, if have multiple episodes may need 2-5yr tx but can be lifelong<br></br>-Can give in depot form if non-compliant (give 2-4wk)<br></br>-May also need adjunctive mood stabilisers (lithium/sodium valproate) and can require concurrent antidepressants (fluoextine)<br></br>-can use PRN benzo (lorazepam) in acute cases of agitation<br></br>-ECT can be indicated for patients with symptoms refractive to mx<br></br>-Other mx includes; screening for co-existing conditions (anxiety, depression, substance use and addiction, personality disorders), addressing psychosocial impact (housing assistance, social skills training, disability support pension, community based mx), addressing psychological factors (suicide prevention, CBT and psychotherapy, family psychotherapy and support)<br></br>-address co-morbidities--> metabolic syndrome monitoring, LFT, FBC, cardiac function, depression, anxiety, substance abuse</p>

112
Q

<p>What are the usual causes for relapse of a mental health condition</p>

A

<p>-Poor adherence to therapy<br></br>-Inadequate drug levels (measure blood)<br></br>-Substance abuse<br></br>-Antidepressent use (SSRI can trigger mania)<br></br>-Stressful life event</p>

113
Q

<p>What is the inclusion criteria for MHA<br></br>What is the exclusion criteria for the MHA</p>

A

<p>Inclusion; patient needs to have a condition characterised by clinically significant disturbances of thought, mood, perception or memory<br></br>-Patient needs tonot have capacity to consent to being treated + the abscence of involuntary tx is likely to result in imminent serious harm to the person or others OR result in the person suffereing serious mental or physical deterioration AND there are no other less restrictive ways to treat the person<br></br><br></br>Exclusion; Doesn't cover people who's odd behaviour/distirbances areattributed to; drugs + alcohol, intellectual disability, antisocial or illegal behaviour, experiencingfamily conflict, influenced by religious/cultural/politicial/philosophical beliefs or displaying immoral/indecent conduct<br></br></p>

114
Q

<p>What are the definitions of the following legal powers<br></br>EEO= emergency examination order<br></br>RR= Request and recommendation<br></br>ITO= involuntary treatment order<br></br>JEO= justice examination order</p>

A

<p>EEO= emergency examination order- can be applied by a police officer or ambulance officer if they think the persons behaviour is at immediate risk of harm to self or others and the risk is secondary to e mental health condition/disability/substance AND the person requires urgent examination and care<br></br>-leads to involuntary examination (12 hours)<br></br><br></br>RR= Request and recommendation<br></br>-if the doctor believes the person is unwell they can put in for a request for assessment or a recomendation for assessment (RA)--> a request for assessmentlast 72 hours and means the patient has to be reviewed by a psychiatrist BUT a recommendation for assessment can last 7 days<br></br><br></br>ITO= involuntary treatment order = Treatment authority<br></br>-can be authorised by the doctor who reviewed the patient after the RA and if they think the patient has fulfilled the criteria for involuntary t<br></br>-has to be reviewed by the mental health tribunal after 4 weeks and then every 6m if the tx is ongoing</p>

<p><br></br>JEO= justice examination order<br></br>-requested by magistrate or JOP- can last 7 days<br></br>-involves a doctor/mental health practitioner travelling to the patient and assessing them, can then determine whether they need an RA</p>

115
Q

<p>What is the definition of capacity<br></br>-4 components</p>

A

<p>-Everyone has capacity until proves otherwise<br></br>4 components; patients needs to have understanding of all the options available, appreciation of the risks and benefits, reasoning and ability to communicate choice</p>

<p>-For a patient to have capacity to consent they need to have an understanding that they have an illness/symptoms that affect their mental health and wellbeing, need to understand the nature and purpose of the teatment, needs to know the risks and benefits of tx and also te consequences of not recieving tx --> they then need to make a decision about tx and communicate their decision</p>

116
Q

<p>What is the difference between an;<br></br>Acute stress disorder<br></br>Adjustment disorder<br></br>PTSD</p>

A

<p>Acute stress disorder - trauma <1 month ago and symptoms last <1month</p>

<p>Adjustment disorder - trauma <3 months ago (and usually not life threatening) and symptoms last <6 months</p>

<p>PTSD - lasts >1 month</p>

117
Q

<p>What is body dysmorphia<br></br>What is muscle dysmorphia<br></br>-Mx for both</p>

A

<p>Body dysmorphia=</p>

<p>-Preoccupation with 1+ defect in appearance not obvious to anyone else</p>

<p>-Repetitive behaviours or mental acts in response to concern (mirror checking, reassurance seeking etc.)</p>

<p>-Significant distress or functional impairment</p>

<p>-Not explained by an eating disorder</p>

<p>Clinical features;</p>

<p>-Defect either minimal or completely imagined with strong beliefs they are unattractive or repulsive<br></br>-Common complaints; muscle, skin defects (acne, scars, wrinkles), hair (thinning or excessive), nose, eyes, teeth, stomach, breasts</p>

<p>-Associated repetitive behaviours; applying foundation, hats/scarves/lots of clothing, repeatedly touching the area, seeking reassurance<br></br>-High rates of suicide<br></br></p>

<p>Muscle dysmorphia;<br></br>-Subset occurring mainly in males<br></br>-Preoccupation that body is insufficiently lean or muscular - usually normal or very muscular<br></br>-Excessively exercise, diet or use anabolic steroids</p>

<p><br></br>Management;</p>

<p>SSRIs</p>

<p>CBT</p>

<p></p>

<p></p>

<p></p>

<p></p>

118
Q

<p>What are the RF for refeeding sx<br></br>-What is the path of refeeding x<br></br>-symptoms<br></br>-how is it prevented<br></br>-how is it managed</p>

A

<p>RF; BMI less than 16, pre-existing low levels of K/Mg/PO4, weight loss more than 15% in last 6 months, little to no nutrient intake for past 10 days</p>

<p></p>

<p>Path; starved patient--> loss of electrolytes intracellularly/intracellular space shrinks but extracellular space retains electrolytes--> introduction of glucose means activation of insulin which moves glucose/K/Mg/PO4 across into intracellular space--> causes drop in serum electrolytes</p>

<p>Prevent;</p>

<p>6000kJs/day initially increasing 2000kJ every 3 days</p>

<p>Via continuous NG tube</p>

<p>Supplemental phosphate &amp; thiamine</p>

<p></p>

<p>Mx;<br></br>-Slowly refeed over weeks<br></br>-Monitor electrolytes regularly and replace as indicated</p>

<p></p>

<p>Symptoms; loss of deep tendon reflexes, arrhythmias, seizures, resp, distress, anaemia, GI sx, hypotension, weakness, lethargy<br></br></p>

119
Q

<p>What is the screening questionairre for anorexia<br></br>-differentials for AN/BN</p>

A

<p>SCOFF<br></br>S= have you ever made yourself SICK because you feel uncomfortably full<br></br>C=do you feel like you have lost CONTROL<br></br>O=have you lost ONE stone (6.3kg) in the past 3 months<br></br>F= do you believe you are FAT when others say you are thin<br></br>F= has FOOD taken over your life<br></br>-score of 2 or more indicates potential AN/BN and requires investigation</p>

<p></p>

<p>DDX;<br></br>-hyperthyroidism, addisons disease, malignancy, coeliac disease, IBD, systemic rheum disease</p>

120
Q

<p>What are the complications of chronic alcoholism</p>

A

<p>GI;</p>

<p>Liver failure - AFLD &amp; cirrhosis</p>

<p>Pancreatitis</p>

<p></p>

<p>HAEM;</p>

<p>Thiamine/B12/folate deficiency*</p>

<p>Macrocytic anemia</p>

<p>Pancytopenia</p>

<p>Hypoglycaemia &amp; ketoacidosis</p>

<p></p>

<p>NEURO;</p>

<p>Withdrawal syndrome</p>

<p>TBI - risk of injury</p>

<p>Wernicke's encephalopathy &amp; Korsakoff's psychosis</p>

<p>Wernicke's - confusion, ophthalmoplegia (diplopia), ataxia, thoughts (memory loss) --> reversible</p>

<p>Korsakoff's - retrograde amnesia, anterograde amnesia, confabulation, apathy --> irreversible</p>

<p>Peripheral neuropathy (alcohol + thiamine deficiency)-->Symmetrical polyneuropathy, Sensory - painful paraesthesias (main Sx), numbness, glove-and-stocking, Motor - cramps, weakness, gait abnormalities</p>

<p></p>

<p>PSYCH;</p>

<p>Depression &amp; anxiety</p>

<p>Suicide</p>

<p></p>

<p>CVS- dilated cardiomyopathy, HTN, AF</p>

<p></p>

<p>RESP- ↑risk of pneumonia</p>

<p></p>

<p>MSK -gout</p>

<p></p>

<p>NEOPLASM- throat, oral, hepatic</p>

121
Q

<p>What is the mx for acute alcohol intoxication presenting to ED</p>

A

<p>o Primary survey (assume OD if unconscious)</p>

<p>· D - don PPE, safe to approach</p>

<p>· R - AVPU</p>

<p>· S - ED reg if worried</p>

<p>· A- assess airway, temporary measures if required, intubate if required (not maintaining or aspiration)</p>

<p>· B - assess respiration, SpO2, start O2 15L non-rebreather if hypoxic</p>

<p>· C - assess circulation, P/BP/ECG, IV access and fluids</p>

<p>· D - look for TBI, BGL &amp; treat hypoglycaemia, eye exam (raised ICP, opioids?)</p>

<p>· E - look for trauma or injury</p>

<p>o Rx</p>

<p>· Thiamine 300mg IV</p>

<p>· Commence AWS</p>

<p>· Admit if withdrawal symptoms - diazepam + thiamine + AWS + sedation score</p>

<p>o Supportive care</p>

<p>· Manage behavioural disturbances - de-escalation, chemical &amp; physical restraints</p>

<p>· Fluids</p>

<p>o Monitor</p>

<p>· Airway &amp; vitals</p>

<p>· Observe until BAC = at least 0.2%</p>

<p>· Withdrawal may begin at BAC = 0.1%</p>

<p>o Closing</p>

<p>· Referral - ATODs, child safety, GP for long-term management (below)</p>

<p>Follow-up - GP</p>

122
Q

<p>What is the mx of alcohol withdrawal</p>

A

<p>o Active</p>

<p>·Thiamine--> IM or IV 300mg TDS (poorly absorbed by GIT) for 3-5 days then 300mg PO for weeks (longer if relapse)</p>

<p>o Check glucose is normal before and give before glucose - otherwise may precipitate Wernicke's</p>

<p>Benzodiazepines--> Diazepam</p>

<p>o Benefits - rapid onset + long half-life, symptomatic relief, prevention and treatment of seizures</p>

<p>o Use (dose depends on severity): diazepam 20mg PO every 2 hours until symptoms subside (60mg max)</p>

<p>o Taper down over 2-7 days then cease completely after 7</p>

<p>o Monitor using AWS &amp; sedation score</p>

<p>o If poor liver function use a benzo that bypasses the liver (LOT- lorazepam, oxazepam, temazepam)</p>

<p></p>

<p>o Supportive</p>

<p>· Fluid balance</p>

<p>· IVFs</p>

<p>· Analgesia - paracetamol</p>

<p>· Low stimulus environment</p>

<p></p>

<p>o Ongoing monitoring</p>

<p>· Admit to hospital</p>

<p>· Alcohol withdrawal scales</p>

<p></p>

<p>o Follow-up</p>

<p>· Arrange continued alcohol intervention</p>

<p>Bio-psycho-social</p>

123
Q

<p>What is the pharmacological mx of nicotine dependence</p>

A

<p>-NRT- to soothe the cravings but doesn’t contain any harmful substances that are in cigarettes</p>

<p>-Buprorpion-antidepresssantà inhibits reuptake of NA and dopamine</p>

<p>-Varenicline (Champax)- partial nicotinic receptor agonist (to soothe cravings) and partial competitive nicotinic receptor antagonist (to reduce the response to smoked nicotine)à high risk of suicide, depression, insomnia</p>

124
Q

<p>What is the mx of opioid dependence<br></br>-drugs used<br></br>-course<br></br>-time frame for withdrawal<br></br>-symptoms of withdrawal</p>

A

<p>Psychosocial</p>

<p>· Rehabilitation</p>

<p>· CBT</p>

<p>· Counselling</p>

<p>· Community support groups</p>

<p>Pharmacological long-term therapy for dependence (MAINTENANCE)</p>

<p>· Benefits</p>

<p>o Reduce craving</p>

<p>o Reduce withdrawal symptoms</p>

<p>o Reduces euphoric effects of heroin in relapse</p>

<p></p>

<p>Drugs used;<br></br>-LA opioid agonists; methadone, buprenorphine,<br></br>-Can use clonidine (A2 adrenergic agonists= decreased SNS outflow)<br></br>-If inpatient= give 4-6mg of opioid agonist and reassess in 3 hours<br></br>-If outpatient= can do 7 day plan of methadone/buprenorphine- can pick up daily from chemist<br></br>-Manage symptomatically= analgesia, fluids, rest, metoclopramide, diazepam (restlessness)</p>

<p></p>

<p>Time course;<br></br>-heroin withdrawal takes about 5-10 days, onset 6-12 hours post heroin intake, peaks at 24-48h<br></br>-long acting opioids like methoadine take 3-6wks to fully detox- begins 36-48h post drug ingestion</p>

<p></p>

<p>Symptoms;<br></br>-anorexia, N/V, abdo pain, cold and flu symptoms (rhinorrhea, myalgia, arthralgia, cramps, hot and cold flushes), restless legs, diarrhoea, perspiration, dilated pupils, intense cravings<br></br><br></br>Scale;<br></br>COWS= clinical opiod withdrawal scale<br></br>OOWS= objective opioid withdrawal scale<br></br>Subjective opioid withdrawal scale</p>

<p></p>

125
Q

<p>What is the mx of acute opioid overdose</p>

A

<p>o Resuscitation</p>

<p>· A - intubate</p>

<p>· B - ventilation</p>

<p>o Decontamination</p>

<p>· Not indicated</p>

<p>o Antidote- Naloxone - if reduced GCS</p>

126
Q

<p>Clinical features of amphetamines/cocaine<br></br>-mx of acute intoxication<br></br>-mx of withdrawal<br></br>-timeline of withdrawal</p>

A

<p>Hyperactive sx; euphoria, increased concentration, increased SNS (high HR/BP, sweating, midriasis), pressured speech, restlessness<br></br>Pscyhotic sx; can look like schizophrenia- agitation, paranoia, delusions<br></br><br></br>Acute;<br></br>-IV diazepam to control seizures and acute agitation<br></br>-Haloperidol or zuclopenthixol (antipsychotic) for psychosis<br></br>-HTN and HR need calcium channel blockers (don't use B-blockers)<br></br><br></br>Withdrawal;<br></br>-Present with dysphoria, fatigue, restlessness, can cause relapse and suicide<br></br>3 Phases;<br></br>-Crash; day 0-2, fatigue, flat affect, increase sleep and appetitie<br></br>-Withdrawal; day 2-4 (can last up to 10wks), low mood and energy, either increased or decreased sleep, vivid unpleasant dreams, psychomotor retardation or agitation, poor concentration<br></br>-Extinction; occurs weeks to months after, the symptoms of the withdrawal slowly subside<br></br>-Withdrawal is not medically dangerous and no medications have been shown to improve withdrawal - mainstay of management is symptomatic</p>

127
Q

<p>What is the path of Wernicke's encephalopathy<br></br>What are the sx of Wernicke's and Korsakoffs encephalopathy<br></br>-what is the immediate mx of a patient presenting with acute Wernicke's encephalopathy</p>

A

<p>Path= thiamine is stored in the liver but only lasts 18 days--> thiamine def causes decreased activity of thiamine dependent enzymes--> causes neuronal death in neurons w increased metabolic requirements and thiamine turnover (ie. brain)</p>

<p>Wernicke's= COAT (confusion, opthalmoplegia (and nystagmus, non-reactive pupils etc), ataxia (of lower limbs/gait), tremor) --> these are irreversibe</p>

<p>Korsakoff's= RACK (retrograde amnesia, anterograde amnesia, confabulation) --> these are permanent and associated with apathy and decreased response/euphoria to events<br></br><br></br>Mx of acute wernicke's;<br></br>-Immediate recognition of underlying undernutrition<br></br>-BGL, FBC, UEC, CMP, LFT, Tox screen<br></br>-Check for hypo--> give thiamine BEFORE giving glucose<br></br>-Give IM/IV thiamine 100mg for 3-5 days<br></br>-Check for other electrolyte abnormalities<br></br>-Supportive care; rehydration, correction of electrolyte abnormalities, nutritional therapy, ALCOHOL CESSATION</p>

128
Q

<p>What is the difference between an organic brain condition and a mental illness</p>

A

<p>-Organic brain conditions (ie.psychosis in dementia and drug induced psychosis)cause visual hallucinations, often have little or no improvement when antipsychotics are used, vague delusions, moderate insight, thought form more organised</p>

<p></p>

<p>-Mental illness; antipsychotics will have some effect, often present with fixed delusions and more auditory hallucinations, less insight, tangential/circumstantial thought form</p>

129
Q

<p>Differentials for psychosis<br></br>Differentials for delerium</p>

A

<p>Psychosis;<br></br>-Neurological (dementia, delerium, head trauma, CNS infection/bleed, tumours), endocrine (hyper/hypothyroidism, cushings, addisons), metabolic (electrolyte disturbance, VB12 def), illicit drug use/withdrawal, schizophrenia/schizoaffective disorder, depression with psychotic features, BPD<br></br><br></br>Delerium; I WATCH DEATH<br></br>Infection (UTI, pneumonia, meningitis), Withdrawal, Acute metabolic condition (electrolytes, organ failure, acidosis), Toxins/drugs, CNS path (stroke, TIA, seizures), Hypoxia (anaemia, HF, resp failure, hypotension), Deficiencies (B12, folate, thiamine), Endocrine (hyper/hypothyroid, cushings, addisons), Acute vascular (haemorrhage, hypertensive encephalopathy), Trauma (head injury, chronic pain), Heavy metals (lead, mercury), Gastointestinal (constipation),</p>

130
Q

<p>Delerium<br></br>-History/exam<br></br>-Ix<br></br>-Imaging<br></br>-How to assess severity<br></br>-mx</p>

A

<p>Hx; onset, course, duration, change in medications, dehydration, falls, trauma, infection, bowel/bladder function (constipation, UTI), alcohol/drugs (withdrawal), PMHX, medications (anticoag), social Hx, premorbid status<br></br>Full body examination looking for evidence of trauma or infection<br></br><br></br>IX; ECG, BSL, MSU, sputum, FBC, UEC, CMP, LFT, lipids, TFT, B12/Folate, blood cultures, ABG, LP<br></br>+/- CXR, CT brain</p>

<p></p>

<p>Assessing severity; use Confusion Assessment Method (score is 0-7, the higher the score the more severe the delerium) --> looks at inattention, acute onset and fluctuating course, disorganised thinking, altered LOC<br></br>-can also use delerium index, confusional state examination, confusion rating scale</p>

<p></p>

<p>Mx;<br></br>-Treat underlying issue and manage the environment<br></br>-Medications may be required to control anxiety, agitation, aggression, delusions or hallucinations--> oral or IM haloperidol or olanzepine (single dose is usually sufficient)<br></br>-Can give thiamine if cause is unknown<br></br>-AVOID BENZO- can worsen confusion and cause resp depression</p>

<p></p>

131
Q

<p>Dementia<br></br>-Diagnostic criteria<br></br>-History/exam<br></br>-Ix<br></br>-Imaging<br></br>-How to assess severity<br></br>​-mx</p>

A

<p>Diagnostic criteria; memory impairment, 1 or more cognitive disturbances on formal testing (aphasia, apraxia, agnosia, disturbed frontal executive functioning (planning, initiation, judgement, adaptability), sufficient to interfere with ADL's, not delerium or another disorder</p>

<p></p>

<p>History; onset/timing (chronic and progressive=dementia), PMHX (look for potentially treatable conditions- MIND WAVES), explore the sx of dementia (psych-hallucinations/paranoia, mood-depressed/anxious/irritable, behavioural- personality change/safety, cognitive-memory/ADLs/judgement), psychosocial aspect (wills+estate, AHD, residence, financial security, alcohol/drug use)fam hx of dementia<br></br>Risk assessment; suicidal, vulnerable, violence, falls, driving, AWOL<br></br><br></br>Exam; vitals, neuro exam (visual field defects can indicate vasc dementia, upgoing plantars=vasc dementia, focal neurology=SOL, parkinsonism), CVS (RF for vascular dementia), resp/abdo (infective causes- delerium)<br></br><br></br>Ix;MSU dipstick - UTI, Glucose - DM, hypoglycaemia, FBC - anemia, infection, UECs + CMP - electrolyte disturbance, renal function, LFTs - alcohol, liver failure, TFTs - hypothyroid, B12/folate, HIV/syphilis serology (TPPA) - if history suggestive<br></br>-CXR, CT head - all patients rule out structural causes, MRI head - specific diagnosis (AD), K10 +/- ANA/anti-dsDNA - collagen disease</p>

<p></p>

<p>Screening; MMSE (<24=prob dementia), GPCOG (gp assessment of cognition), FAB (frontal assessment battery- <12 prob dementia), ADAS-cog, kimberley indigenous cognitive assesmment, dementia severity rating scale</p>

<p></p>

<p>Mx;</p>

132
Q

<p>Dementia;</p>

<p>What are the treatable types/imitators and what are the primary degenerative types<br></br>-how to distinguish dementia from schizophrenia</p>

A

<p>Primary degenerative; alzheimers, vascular dementia, lewy body dementia, parkinsons dementia, frontotemporal dementia (Picks)<br></br><br></br>Treatable/imitators; MINDWAVES<br></br>Meningioma (or other CNS tumours), infectious (neurosyphilis, HIV, CJD, chronic meningitis), Nephron (uremia, hepatic encephalopathy), Depression/delerium, Wenickes, Alcohol and drugs, Vitamin B12 def, Endocrine (hypothyroidism), Subdural (chronic)</p>

<p></p>

<p>-Dementia occurs in older patients and is associated with a change in cognitive AND behavioural changes</p>

133
Q

<p>What is the purpose of a frontal assessment battery<br></br>-what other cognitive tests can be used in a demented patient</p>

A

<p>-Used to fistinguish fronto-temporal tye dementia from DAT in mildly demented patients (MMSE >24), higher the score the better the performance<br></br>-score of 12-18 indicates frontal lobe dysfunction<br></br>-tests conceptualisation, mental flexibility (naming words starting with S), programming (fist-edge-palm), conflicting instructions (tapping), inhibitory control (don't tap) and environmental autonomy (don't grab my hands)</p>

<p></p>

<p>MMSE<br></br><br></br>Addenbrooks;<br></br>a brief cognitive test that assesses five cognitive domains, namely attention/orientation, memory, verbal fluency, language and visuospatial abilities. Total score is 100, higher scores indicates better cognitive functioning.</p>

134
Q

<p>Explain the following defintions;<br></br>-Somatic symptom disorder; what is it, common presentations<br></br>-Illness anxiety disorder<br></br>-Conversion disorder<br></br>-Factitious disorder<br></br>-Malingering</p>

A

<p>-<strong>Somatic symptom disorder</strong>= somatic symptoms are unconciously produced and there are no physical findings--> suspect a somatasising patient if they complain of multiple symptoms in multiple systems over a 3 month period, will have a history of extensive invesigations which are negative, symptoms often cause disruption of functioning</p>

<p>Common PCs; Pain - diffuse, joint, back etc, CVS - atypical chest pain, palpitations, Resp - dyspnoea, hyperventilation, GIT - unexplained abdominal pain, IBS, Neuro - headaches (tension type), ENT - globus syndrome (lump in throat)</p>

<p></p>

<p><strong>Illness anxiety;</strong>Hypochondriasis; llness preoccupation becomes part of identity --> common topic of discussion and characteristic response to stress, Extensive history of unsatisfactory medical care with repeated negative diagnostic tests, 2/3 have comorbid depressive or anxiety disorder, high level of anxeity about health, illness preoccupation has been present for at least 6 months<br></br>-possible role of SSRI due to extreme anxiety</p>

<p></p>

<p><strong>Conversion disorder;</strong>abrupt onset neurological symptoms which are incompatible with investigation results,Motor - include: weakness, paralysis, psychogenic seizures, abnormal movements, tremor, abnormal posture, difficult swallowing, unable to speak, incontinence, Sensory - include: altered/reduced/loss of skin sensation, hearing or vision</p>

<p></p>

<p><strong>Factitious disorder; Munchausen syndrome-</strong>psychological or physical syptoms that are faked for sympathy or a sick role - patient is not concerned about developing the symptoms or medical condition<br></br><br></br>Malingering; physical or psychological sx are faked for secondary gain (money, medication, leave)</p>

<p><br></br>-Illness anxiety disorder<br></br>-Conversion disorder<br></br>-Factitious disorder<br></br>-Malingering</p>

135
Q

<p>What is a sick role<br></br>What is illness behaviour</p>

A

<p>Sick role; role taken by a patient and is when a person does not have to fulfil their normal roles (work, chores), should seek medical attention and do as doctors say, must try to get well and is not held accountable for their illness</p>

<p></p>

<p>Illness behaviour; the way a person monitors their bodies, fedines and interprets their symptomas and takes remedial action and utilises soures of help --> arise from biological predispositions and the nature of symptomatology/learned pattern of response<br></br>-illness behaviour is affected by gender (most likely F to access healthcare), age, ethnicity, culture, education, family structure, finances, insurance<br></br>-abnorm illness behaviour is a maladaptive manner of experiencing or acting in response to health and illness which is disproportionate to the pathology<br></br><br></br>Primary gain; produces positive internal motivations--> if a dx is present it makes the patient have less psychological distress<br></br>-falsifying symptoms for primary gain is factitious disorder<br></br><br></br>Secondary gain; falsification of symptoms for secondary gain is malingering<br></br>-external motivator--> is if a patients disease allows them to miss work/avoid duties/get financial compensation/obtain drugs</p>