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Year 4C - psych > SJS Psych revision > Flashcards

SJS Psych revision Flashcards

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1
Q

What are the DSM criteria for MDD?

A

5 or more symptoms (with at least one of 1 or 2) in a two week period and represents a change of normal. Needs to be most of the day nearly every day.

  1. Depressed mood
  2. Anhedonia
  • Weight loss/gain
  • Insomnia/hypersomnia
  • Psychomotor agitation/retardation
  • Fatigue
  • Worthlessness/guilt
  • Decreased concentration
  • Suicidal ideation

Additional features/subtypes

  • Anxious distress
  • Melancholic features
  • Psychotic features
  • Catatonic (more common in schizophrenia)
  • Seasonal pattern
  • Postpartum
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2
Q

What are the criteria for bipolar disorder?

A

Elevated, irritable or elated mood PLUS

3 or more symptoms of DIG FAST

D - Distractibility

I - Increased risk taking

G - Grandiosity
F - Flight of ideas
A - Activity – increased psychomotor activity

S - Sleep – decreased need

T - Talkative

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3
Q

What are the DSM criteria for schizophrenia?

A

Overall disturbance for at least 6 months

Two or more of the following over 1 month. Must have at least 1 of 1-3

  1. Delusions
  2. Hallucinations
  3. Disorganised speech
  4. Grossly disorganised or catatonic behaviour
  5. Negative symptoms - the 6 As
  • Blunted Affect
  • Anhedonia
  • Alogia (poverty of speech)
  • Avolition (decreased motivation)
  • Poor Attention
  • Asocial features
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4
Q

What is the DSM timeframe for brief psychotic disorder?

A

1+ days but <1month

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5
Q

What are the criteria for delusional disorder?

A
  • The presence of one (or more) delusions with a duration of 1 month or longer.
  • Criterion A for schizophrenia has never been met.
    • Note: Hallucinations, if present, are not prominent and are related to the delusional theme (e.g., the sensation of being infested with insects associated with delusions of infestation).
  • Apart from the impact of the delusion(s) or its ramifications, functioning is not markedly impaired, and behavior is not obviously bizarre or odd.
  • If manic or major depressive episodes have occurred, these have been brief relative to the duration of the delusional periods.
  • The disturbance is not attributable to the physiological effects of a substance or another medical condition and is not better explained by another mental disorder, such as body dysmorphic disorder or obsessive-compulsive disorder.
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6
Q

What is factitious disorder?

A

A factitious disorder is a condition in which a person acts as if they have an illness by deliberately producing, feigning, or exaggerating symptoms. Factitious disorder imposed on another is a condition in which a person deliberately produces, feigns, or exaggerates symptoms in a person in their care.

Münchausen syndrome, a severe form of factitious disorder, was the first kind identified, and was for a period the umbrella term for all such disorders.

People with this condition may produce symptoms by contaminating urine samples, taking hallucinogens, injecting themselves with fecal material to produce an abscess, and other similar behaviour.

The deceptive behavior is evident even in the absence of obvious external rewards.

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7
Q

What are the criteria for somatic symptom disorder?

A
  • One or more somatic symptoms that are distressing or result in significant disruption of daily life.
  • Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associated health concerns as manifested by at least one of the following:
  • Disproportionate and persistent thoughts about the seriousness of one’s symptoms.
  • Persistently high level of anxiety about health or symptoms.
  • Excessive time and energy devoted to these symptoms or health concerns.
  • Although any one somatic symptom may not be continuously present, the state of being symptomatic is persistent (typically more than 6 months).
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8
Q

What are the criteria for illness anxiety disorder?

A
  • Preoccupation with having or acquiring a serious illness.
  • Somatic symptoms are not present or, if present, are only mild in intensity. If another medical condition is present or there is a high risk for developing a medical condition (e.g., strong family history is present), the preoccupation is clearly excessive or disproportionate.
  • There is a high level of anxiety about health, and the individual is easily alarmed about personal health status.
  • The individual performs excessive health-related behaviors (e.g., repeatedly checks his or her body for signs of illness) or exhibits maladaptive avoidance (e.g., avoids doctor appointments and hospitals).
  • Illness preoccupation has been present for at least 6 months, but the specific illness that is feared may change over that period of time.
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9
Q

What are some of the key features of vascular dementia?

A
  • ‘A step wise progression’
  • Risk factors for vascular disease
  • Initially memory sparing
  • Typically executive function affected
  • Behaviour change
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10
Q

What are some of the key features of Lewy Body dementia?

A
  • Rapid onset
  • Rapid progression
  • Fluctuating mental state and cogniton - like delerium
  • Visual hallucinations
  • Postural instability
  • Reversed sleep wake cycle
  • Soft Parkinson’s symptoms
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11
Q

A patient is on an antidepressant and has raised LFTs and a low WCC. What drug are they on?

A

Mirtazipine

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12
Q

What main medication do you give for neuroleptic malignant syndrome?

A

bromocriptine

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13
Q

What are the hallmarks of oppositonal defiant disorder?

A

The essential feature of oppositional defiant disorder is a frequent and persistent pattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness (Criterion A of DSM).

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14
Q

What are the principles of management of oppositional defiant disorder?

A
  • Three principles of treatment are important:
    • Psychotherapy is the preferred first-line treatment
      • A specialized therapy technique called parent management training (PMT) teaches parents ways to positively alter their child’s behavior.
    • careful assessment and treatment of comorbid conditions is essential
    • there is a limited role for pharmacological treatment
      • Risperidone has an approval in Australia for the treatment of conduct and other disruptive behaviour disorders in those with intellectual disability in whom destructive behaviours (eg aggression, impulsivity and self-injurious behaviours) are prominent
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15
Q

What are the main features of conduct disorder?

A

The essential feature of conduct disorder is a repetitive and persistent pattern of behavior in which the basic rights of others or major age-appropriate societal norms or rules are violated.

Typically more severe behavior c.f. oppositional defiant disorder, and includes aggression toward people or animals, destruction of property, or a pattern of theft or deceit.

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16
Q

What % of dementia (in Western countries) is caused by Alzheimers?

A

60-70%

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17
Q

What are the key features of frontotemporal dementia?

A
  • Personality change and alteration in behaviour are the earliest manifestations of the condition. Social disinhibition and insightlessness may be a problem.
  • A small number of frontal dementia patients present with word finding difficulty, which progresses to a profound nonfluent dysphasia (semantic dementia).
  • Many patients with a frontal dementia are apathetic and withdrawn, especially in the later stages of the illness. As the dementia progresses, memory deficits may become more prominent.
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18
Q

A patient comes to you with terrible depression. They say that they want the strongest treatment you’ve got. They don’t care about side effects they just want the depression gone, now. What do you prescribe?

A

“California rocket fuel” is a medical slang term for the combined administration of Mirtazapine (a NaSSA) and Venlafaxine (an SNRI).[1] This combination is usually used in the treatment of severe and/or treatment-resistant depression and has superior efficacy to tranylcypromine,

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19
Q

What are the causes of treatment failure in psychiatry?

A

IM STILL SAD

I - Incorrect diagnosis
M - Medical causes not excluded
S - Side effects intolerable
T - Time inadequate (e.g. 4-6 weeks for antidepressant)
I - Interactions (CYP450)
L - Low dose
L - Lifestyle factors
S - Social support poor
A - Adherence to treatment?
D - Drugs with psych problems - alcohol, cannabis, methamphetamines etc

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20
Q

What are the side effects of SSRIs?

A

“DASHINS” (like dashing but dashins)

  • *D**iarrhoea
  • *A**nxiety

Suicide

  • *H**eadache
  • *I**nsomnia
  • *N**ausea

Sexual dysfunction

Also hyponatraemia and serotonin syndrome!

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21
Q

What are the side effects of SNRIs?

A

“DASHINS” (like dashing but dashins)

  • *D**iarrhoea
  • *A**nxiety

Suicide

  • *H**eadache
  • *I**nsomnia
  • *N**ausea

Sexual dysfunction

Also hyponatraemia, palpitations, tachycardia, hypertension and serotonin syndrome!

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22
Q

What are the side effects of TCAs?

A

In addition to SSRI adverse effects:

Anticholinergic (atropine-like) effects: blurred vision, dry mouth, urinary retention, constipation and narrow angle glaucoma.

Sympatholytic effects (alpha 1 blockade): postural hypotension, dizziness and reflex tachicardia.

Histamine (H1) antagonism: sedation.

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23
Q

You have been asked by your consultant to start Jim on sertaline for depression. What are the standard things you tell a patient before starting them on an SSRI/SNRI?

A
  1. You might need to try more than one before you find the one that suits you best — not everyone responds the same way to a particular antidepressant.
  2. They take a while to work
    1. Often you will start to feel better within 1 to 3 weeks of starting an antidepressant, but it can take 6 to 8 weeks to feel the full effect.
  3. Some side effects are temporary, others are not
    1. All antidepressants have side effects; some might go away after a few weeks (e.g. insomnia, nausea, dizziness), while others may not (e.g. sexual problems).
  4. Come back and let us know if you have side effects
  5. Take the full course to keep depression away
    1. Keep taking your antidepressant after you start to feel better for as long as your doctor advises (usually 6 to 12 months) — this will reduce the risk of your depression coming back when you stop treatment.
  6. Don’t stop suddenly
    1. With most antidepressants, stopping them suddenly can cause symptoms such as dizziness, nausea or feeling jittery. When it’s time to stop taking your antidepressant, your doctor will usually need to reduce the dose gradually over at least a few weeks.
  7. Know which medicines interact
    1. Some antidepressants increase the amount of serotonin (a neurotransmitter or brain chemical). Combining these antidepressants with other medicines or illegal drugs that also increase serotonin can cause a serious reaction called serotonin syndrome or serotonin toxicity.
  8. Try psychological therapy first for mild depression
    1. For mild depression, it’s better to try psychological therapies first, because they are more effective than antidepressants in this situation.
  9. The effects of CBT last longer
    1. Cognitive behavioural therapy (CBT), a talking therapy, is about as effective as antidepressants for moderate depression, but the benefits may last longer.
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24
Q

Which drugs are your first line for negative symptoms of schizophrenia?

A

amisulpride or clozapine

and

fluoxetine

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25
Q

What are some of the risks and side effects of clozapine?

A

Sedation - 40%

Neutropenia - 2% to 3%

Agranulocytosis - 1%

Myocarditis/cardiomyopathy

Gastrointestinal hypomotility - Ranging from constipation to bowel perforation and death

Urinary retention

Urinary incontinence

Hypersalivation with risk of aspiration pneumonia

Orthostatic hypotension

Myoclonus and seizures

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26
Q

What are the main dopaminergic pathways in the brain and what function do they serve?

A

Mesocortical

Motivation and emotion

Negative symptoms of schizophrenia

Mesolimbic

“Reward pathway”

Positive symptoms of schizophrenia

Nigrostriatal

Movement pathway

Extrapyramidal symptoms

Hypothalamic/ tubuloinfundibular

Connection to posterior pituitary

Regulation of prolactin

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27
Q

Explain the basic pathophysiology of the adverse effects of antipsychotics

A

In short, ideally we want to inhibit dopaminergic activity in the mesocortical and mesolimbic pathways, but NOT the nigrostriatal and hypothalamic pathways, as inhibition in these pathways causes side effects. Unfortunately however, none of the drugs we have are specific to the mesocortical and mesolimbic pathways and thus it is important to understand the effects of dopamine blockade in these other pathways.

The adverse effects of antipsychotics are either due to their inhibition of dopamine in pathways other than the mesocortical/mesolimbic, or their blockade of other non-dopaminergic receptors. Antipsychotics vary in how “messy” they are – ie: how selective for D2 receptors they are.

Side effect

Related to

Mechanism

Extrapyramidal side effects (EPSE)

Dopamine blockade

Nigrostriatal D2 blockade

Gynacomastia/ amenorrheoa

Hyperprolactinaemia from loss of dopaminergic inhibition of the hypothalamus

Sedation

Messy drug. Blockade of other receptors types.

Histamine (H1) blockade

Postural hypotension

a1 blockade

Dry mouth, blurred vision, constipation

Muscarinic blockade

Weight gain

5HT2 blockade

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28
Q

How do you conceptualise of the different antipsychotics and their side effect profiles?

A

High potency

(Doses <10mg)

Low potency

(Doses >100mg)

Typical

Haloperidol

Zuclopenthixol

Chlorpromazine

Highest risk of EPSE

Atypical

Risperidone

Aripiprazole

Quetiapine

Clozapine

Amilsulpride

Olanzapine* (*breaks the rule!)

Highest risk of metabolic syndrome (hyperlipidaemia, weight gain, DM)

Highest risk of EPSE

Highest risk of sedation, hypotension, anticholinergic effects

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29
Q

What is the pathophysiology of EPSE?

A

It is important to understand that dopamine and acetylcholine are in competitive balance in several key brain pathways. Inhibiting dopamine receptors with antipsychotics effectively increases the concentration of unopposed acetylcholine –> this is the underlying mechanism of an important group of antipsychotic side effects known as extrapyramidal side effects (EPSE).

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30
Q

What are the extrapyramidal side effects?

A

This relative excess of Ach is the underlying mechanism of EPSE. The classic EPSE are:

  • dystonia (continuous spasms and muscle contractions)
  • akathisia (motor restlessness)
  • akinesia/parkinsonism (rigidity, bradykinesia, and tremor), and
  • tardive dyskinesia (irregular, jerky movements).

Acute dystonia

Akasthisia

Akinesia

Tardive dyskinesia

Typical onset

4 hours

4 days

4 weeks

4+ years

Remember

‘Muscle’

‘Rustle’

‘Hustle’

IRREVERSIBLE!

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31
Q

What is the management of EPSE?

A

Treatment of EPSE:

  1. Cease/reduce dose of causative drug
  2. Rx anticholinergic –> benztropine
  3. Akathisia may require beta-blockers or even benzodiazepines.
32
Q

Why are some antipsychotics more or less likely than others to cause EPSE?

A

One particularly important pharmacologic action of some typical antipsychotics is their ability to block muscarinic M1-cholinergic receptors. This can cause undesirable side effects such as dry mouth, blurred vision, constipation, and cognitive blunting. Differing degrees of muscarinic cholinergic blockade may also explain why some typical antipsychotics have a lesser propensity to produce extrapyramidal side effects (EPS) than others. That is, those typical antipsychotics that cause more EPS are the agents that have only weak anticholinergic properties, whereas those typical antipsychotics that cause fewer EPS are the agents that have stronger anticholinergic properties.

33
Q

What are the signs and symptoms of neuroleptic malignant syndrome?

When does it typically occur?

A

It is a potentially fatal condition characterised by:

  • fever
  • marked muscle rigidity
  • altered consciousness
  • autonomic instability

NMS usually progresses rapidly over 24–72 hours. Not all typical signs need to be present for diagnosis. The incidence of NMS is greatest in young men. It does not always occur immediately after starting antipsychotic treatment, and may be seen after many months or years.

34
Q

What monitoring do patients on antipsychotics need and how often?

A

Every visit

Weight and waist circumference

Adverse effects

Smoking

Alcohol

Every 6 months

EPSE screen

Annually (or every six months if on olanzapine)

BP

Fasting lipids

Fasting BGL

Prolactin levels

35
Q

What are the side effects of lithium?

A

There are a lot of side effects but the ones to know are:

  • Metallic taste
  • GI side effects
  • Weight gain
  • Nephrotoxicity
  • Benign T wave changes on ECG
  • Exacerbation of dermatologic conditions and
  • Thyroid dysfunction.

The serious complication is lithium toxicity

36
Q

What are the signs and symptoms of lithium toxicity?

A

Mild-to-moderate

Blurred vision, increasing diarrhoea, nausea, vomiting, muscle weakness, drowsiness, apathy, ataxia, flu-like illness.

Severe

Increased muscle tone, hyper-reflexia, myoclonic jerks, coarse tremor, dysarthria, disorientation, psychosis, seizures, coma.

37
Q

What is the therapeutic range of lithium?

A

Acute mania: 0.5–1.2 mmol/L

Prophylaxis: 0.4–1 mmol/L

38
Q

What drugs do you use for acute behavioural disturbance?

A
39
Q

Describe the mainstays of treatment of detox from opiods…

A
  1. Detox

Medical management of withdrawal symptoms using buprenorphine (a partial opioid agonist), with or without cautious use of diazepam

Withdrawal often resolves over 10 days

This is best done as an inpatient at a specialized detox service, but it can be done in the outpatient setting

Initial success rates are high, but relapse is extremely common

  1. Replacement

Methadone

An oral opioid tablet that does what heroin dose (therefore stops withdrawal)

Initially dispensed daily from a pharmacy, then dosing can be stretched out depending on success

Reduces drug associated infection risk, crime and the financial burden

Usually used as long term replacement, not particularly good for coming off opioids altogether

Buprenorphine

A partial opioid agonist, comes as a sublingual spray

Can be used long term, or for tapering down and eventual cessation

Comes in two forms, one with buprenorphine alone (Subutex) and one with naloxone (Soboxone), with blocks opioid action if taken IV. With soboxone, it stops you from dissolving the drug and injecting it. Naloxone is inactive via sublingual administration

40
Q

What are the complications of using opiods in pregnancy?

A

Before birth

  • When you have withdrawal, you baby does to
  • Heroin withdrawal in the infant increases the risk of miscarriage, premature labour and stillbirth.
  • Injecting heroin increases the risk of blood borne viruses (HBV, HCV, HIV) which can affect the baby
  • Heroin is often mixed with other chemicals, the safety of these chemicals for the baby cannot be known
  • Methadone stabilistion of opioid use is recommended and safe

After birth

  • heroin can enter the breastmilk; breast feeding is not recommended
  • The child may have withdrawal after birth (neonatal abstinence syndrome) and will need to be admitted and monitored for 7 days
  • The risk of SIDS is increased
41
Q

What is the first line drug for anxiety disorders?

A

Escitalopram

42
Q

What is Russel’s sign?

A

Russell’s sign, named after British psychiatrist Gerald Russell, is a sign defined as calluses on the knuckles or back of the hand due to repeated self-induced vomiting over long periods of time.

43
Q

What is the diagnostic triad of normal pressure hydrocephalus?

What is the mainstay of treatment?

A

Wet, wobbly and wacky

Gait ataxia unresponsive to a trial of levodopa

Cognitive decline

Bladder incontinent

The gait ataxia usually comes on first and looks similar to Parkinsons –> festination, stuck in doorways etc

Mainstay of treatment is VP shunt

44
Q

What kind of hallucinations are classically seen in delerium tremens?

A

Examples of visual hallucinations include insects crawling on self or animals circling the bed.

Tactile hallucinations include sensation of pins or electric shocks all over the body and insects crawling on the skin.

45
Q

A 50yo man known to have moderate-severe alcoholism has been brought to ED with decreased conscious state. You immediately order a BGL and find it to be 1.8. You need to get IV access and give him some 5% glucose for his hypoglycaemia and (presumed) dehydration but what must you do first?

A

Always give thiamine before administering glucose (including dextrose 5% IV) for hypoglycaemia.

Give thiamine before administering glucose (including intravenous 5% dextrose) for hypoglycaemia because giving glucose in the presence of thiamine deficiency may precipitate Wernicke’s encephalopathy.

46
Q

What is the most severe form of acute alcohol withdrawal syndrome?

What are the symptoms?

What is the management?

A

Alcohol withdrawal delirium (also known as delirium tremens) is the most severe manifestation of alcohol withdrawal syndrome.

Symptoms

Commences 72 to 96 hours after cessation of drinking and is characterised by gross tremors and fluctuating levels of agitation, hallucinations (usually tactile and visual), disorientation and impaired attention.

Fever, tachycardia and dehydration may be present.

Management

It is a medical emergency that always requires hospitalisation and, if inadequately treated, has a high mortality rate, mainly from heart failure. Alcohol withdrawal delirium is rarely uncomplicated; it is usually associated with infections, anaemia, metabolic disturbances and head injury. It may be associated with a range of other disorders including Wernicke’s encephalopathy and hepatic encephalopathy.

Treat with admission, monitoring, benzos, thiamine and haloperidol PRN for hallucinations.

47
Q

What is the cause of Wenicke-Korsakoff syndrome?

What are the symptoms?

What is the management?

A

Cause

Wernicke’s encephalopathy is a life-threatening complication of thiamine deficiency, characterised by ophthalmoplegia, ataxia and confusion. It is generally associated with chronic alcohol use, but also occurs in association with bariatric surgery, cancer and recurrent vomiting or chronic diarrhoea.

Korsokoff syndrome/Korsakoff psychosis is a result of long term severe thiamine deficiency. It is defined as an anterograde amnestic syndrome with disproportionate impairment of recent memory relative to other cognitive domains, accompanied sometimes with confabulation. It can occasionally occur without a preceding Wernicke’s encephalopathy.

Symptoms

Wernicke encephalopathy

Opthalmoplegia, ataxia, frank confusion, impaired cognition, apathy.

Can present with psychosis and delerium and be mixed in with Delerium Tremens.

Korsakoff syndrome

An acute onset of severe memory impairment without any dysfunction in intellectual abilities.[1][5] The DSM IV lists the following criteria for the diagnosis of Korsakoff’s Syndrome:

  • anterograde amnesia
  • Variable presentation of retrograde amnesia
  • One of:
    • Aphasia
    • Apraxia
    • Agnosia
    • A deficit in executive functions

Management

Wernicke encephalopathy

Immediate therapy is required to minimise irreversible neurological damage with progression to Korsakoff’s psychosis.

Resus/secure airway, circulation etc

High dose IV thiamine, magnesium and multivitamins

48
Q

What are the DSM criteria for adjustment disorder?

A

The development of emotional or behavioral symptoms in response to an identifiable stressor(s) occurring within 3 months of the onset of the stressor(s).

These symptoms or behaviors are clinically significant, as evidenced by one or both of the following:

  • Marked distress that is out of proportion to the severity or intensity of the stressor, taking into account the external context and the cultural factors that might influence symptom severity and presentation.
  • Significant impairment in social, occupational, or other important areas of functioning.

The stress-related disturbance does not meet the criteria for another mental disorder and is not merely an exacerbation of a preexisting mental disorder.

The symptoms do not represent normal bereavement.

Once the stressor or its consequences have terminated, the symptoms do not persist for more than an additional 6 months.

49
Q

What drugs do you use for the various presentations of bipolar disorder?

A
50
Q
A
51
Q

What are the basic differentials for cognitive decline in the elderly?

A

5Ds

Dementia

  • Frontrotemporal dementia
  • Lewy-Body Dementia
  • Alzheimer’s disease
  • Parksinon’s related
  • Alcohol related
  • Vascular dementia

Depression

Delirium

Diseases (Parkinson’s / Huntington’s)

Disguises (reversible causes of reduced congition).

  • brain tumor
  • sub dural haemorrhage
  • normal pressure hydrocephalus
52
Q
A
53
Q

An elderly woman presents with cognitive decline and you need to rule out organic causes before diagnosing her with dementia (major neurocognitive disorder). You know you need to perform an “old people screen”. What tests does this include?

A
  • FBE
  • UEC / CMP
  • LFT
  • BGL
  • TFTs
  • B12 and folate levels
  • Syphillis serology
  • CXR
  • CTB / MRI brain
  • Geriatric Depression Scale
54
Q

You have just diagnosed Mr. Green with a major neurocognitive disorder. What services can you refer him and his family to?

A
  • ACAS [Aged Care Assessment Service]: a multidisciplinary assessment of Clarence and his wife in their home environment.
  • CDAMS [Cognitive, Dementia and Memory Service] for specialist diagnosis and opinion on management
  • Local branch of Alzheimer’s Australia for provision of information, care advice, support groups and counseling as required
  • Dementia Behaviour Management Advisory Service (DBMAS), which has a 24-hour helpline with trained staff who can advise on strategies to manage challenging behaviours in people with dementia.
  • VicRoads for medical form and OT assessment
55
Q

How do you determine if a patient has Lewy Body Dementia or Dementia Associated with Parkinson’s Diease?

A

LBD is distinguished from the dementia that sometimes occurs in Parkinson’s disease by the time frame in which dementia symptoms appear relative to Parkinson symptoms.

Parkinson’s disease with dementia (PDD) would be the diagnosis when dementia onset is more than a year after the onset of Parkinson’s.

LBD is diagnosed when cognitive symptoms begin at the same time or within a year of Parkinson symptoms.

56
Q

What are the three hallmark clinical features of frontotemporal dementia?

How is this presentation different to Alzheimer’s disease?

A
  • Personality change (apathy, disinhibition, loss of insight)
  • Loss of the ability to recognize the meaning of words and objects and
  • Global cognitive decline.

FTDs have an earlier onset (45-65) than AD and, at an early stage, do not cause the memory loss and visuo-spatial disorientation that are so characteristic of AD.

57
Q

You have just diagnosed Rosie’s Dad with dementia and prescribed a cholinesterase inhibitor. Rosie asks how effective this medication is. Rosie is very educated and wants to know all the facts. What do you say?

A
  • Cholinesterase inhibitors offer modest benefits to patients with dementia.
  • These drugs improve alertness and function and can maintain cognitive scores at or above the baseline for up to 12 months; however, they do not modify the underlying progression of pathology.
  • Open-label trials yielded results consistent with continued benefit for up to 4 years. Six-month studies suggest that between five and fifteen patients need to be started on treatment to see a significant improvement in one patient.
  • Not all patients benefit from cholinesterase inhibitors; some have modest benefit and a few show significant improvement. Adverse effects, particularly gastrointestinal, prevent the use of these drugs in some patients.
58
Q

What are the two main cholinesterase inhibitors used for dementia and what is their main side effect?

A

Galantamine prolonged-release

OR

donepezil

The cholinesterase inhibitors are associated with prominent gastrointestinal adverse effects, particularly anorexia, nausea and vomiting.

59
Q

Mrs. Green is 77 years old and has moderate Alzheimers dementia. She is on an anticholinesterase but her family want to know if any other medications may help. What do you say?

The family want to know if there are any side effects if you were to prescribe this drug for Mrs Green, what do you say?

A

NMDA receptor antagonists

Memantine, an antagonist of N-methyl-D-aspartate (NMDA), is approved by the TGA as a treatment for moderate-to-severe Alzheimer’s disease.

Memantine is excreted by the kidney so reduce dose in kidney failure. The drug is usually well tolerated.

60
Q

Mrs Green has severe dementia and is displaying more and more behaviours of concern as her disease progresses. She has been seen by an expert multidisciplinary team who have instituted many behavioural techniques for calming Mrs Green but these have been modestly successful. They have now called you in as the doctor, what medical therapies could you offer?

A

Behavioural and mood disturbances

Should be primarily managed with supportive care measures. If pharmacotherapy is considered necessary to control hallucinations, delusions or seriously disturbed behaviour, use (short term only)

risperidone - 0.25 mg orally, twice daily initially.

To relieve symptoms of severe anxiety and agitation, use:

oxazepam - 7.5 mg orally, 1 to 3 times daily

61
Q

Mrs Smith has been brought to you because her husband thinks that she has Alzheimer’s dementia. A family friend of the Smith’s is a GP and has told Mr Smith that whilst his wife’s symptoms do sound like dementia, they do not sound like Alzheimers dementia. What symptoms/features may Mrs. Smith have that would suggest she has a different type of dementia to Alzheimers?

A

A dementia syndrome with any of the following:

  • sudden onset,
  • focal neurological signs,
  • seizures or gait disturbances early in the course of the illness.
62
Q

What are the MMSE cutoff limits for mild, moderate and severe cognitive impairement?

A

0-10 (severe)

11-19 (moderate)

20-24 (mild)

25+ (normal)

Modified by education and age. So you might adjust the standard rating for a lawyer (or senior lecturer) with a MMSE of 26 for example.

63
Q

You have been asked to perform a MMSE on Mrs Sewell. What do you say to her before you commence the assessment?

A
  • Hi Mrs. Sewell my name’s Scott Santinon, how are you today?
  • Dr. Bartlett has asked me to come and run through some questions with you that relate to your orientation, recall and working memory.
    • Basically what that involves is us spending about 5 to 10 minutes running through a standard screening tool. Does that sound okay?
  • Now Mrs. Sewell I have to of course remind you that everything that we discuss today will remain completely confidential between you and I, but I will of course report back to Dr. Bartlett when we’re finished.
  • Okay thanks Mrs. Sewell, now some of these questions and tasks may seem irrelevant, but it will only take 5 to 10 minutes to go through so if you could bear with me that would be great.
64
Q

How would you perform/score a MMSE without the pro-forma?

A

ORArL 23 RWD

O: Orientation to Place and Time

Year, Season, Month, Date, Day (5)

Country, State, Suburb, Hospital/Street Name, Ward/House Number (5)

R: Recognition

Ball, car, man (3)

A: Attention

WORLD backwards (5)

r: recall

Ball, car, man (3)

L: Language

No ifs, ands, or buts (1)

2:

Watch, pen (2)

3:

Take this paper in your right hand, fold it in half and place it on the floor (3)

R: Reading

“Close your eyes” (1)

W: Writing

Write a sentence (1)

D: Drawing

Copy a figure of two intersecting pentagons (1)

65
Q

What questions would you ask in a substance abuse history?

A
  • Abuse
    • Interpersonal problems
    • Neglecting responsibilities
    • Physical safety
    • Legal problems
  • Dependence
    • Withdrawal symptoms
    • Activities to obtain the substance?
    • Tolerance?
    • Escalating dose/frequency?
    • Difficulty cutting down
66
Q

What questions would you ask in a PTSD history?

A
  • Intrusive thoughts
  • Flashbacks
  • Anxiety symptoms/hypervigilance
  • Detachment
  • Avoidance behaviours
  • Cognitive problems
67
Q

What questions would you ask to screen for symptoms of generalised anxiety disorder?

A
  • Anxiety and worry most of the day, most days of the week for >6 months
  • Can’t control the worry
  • Irritability
  • Muscle tension
  • Easily fatigued
  • Sleep disturbance
68
Q

How will you set up your page for a psych history?

A
69
Q

Which SSRI has the lowest risk of hyponatraemia?

A

Escitalopram

70
Q

Which SSRI is least likely to cause weight gain?

A

Escitalopram

71
Q

What are the signs/symptoms of TCA overdose?

A

Altered conscious state

Tachycardia

Hypotension

Dilated pupils

Warm, flushed, dry skin

Acute urinary rentention and constipation

Ataxia, hypereflexia

72
Q

What are the two main investigations (and related findings) in TCA overdose?

A

ECG –> tachycardia and wide QRS

ABG –> metabolic acidosis

73
Q

What are the core features of management of TCA overdose?

A

Resucitation

Activated charcoal

Sodium bicarbonate infusion to correct wide QRS

74
Q

What are the criteria that a patient needs to meet in order for you to make an Assessment Order?

A
  1. The patient appears to have a mental illness
  2. Because of that mental illness the person appears to need immediate treatment to prevent
    • serious deterioration in the person’s mental or physical health
    • serious harm to the person or to another person
  3. if the person is made subject to an assessment order, the person can be assessed
  4. there is no less restrictive means reasonably available to enable the person to be assessed.
75
Q

What are the criteria a patient needs to be meet for you to make them a Treatment Order?

A
  1. The person has a mental illness
  2. Because the person has a mental illness, the person needs immediate treatment to prevent:
    • Serious deterioration in the person’s mental or physical health,
    • Or serious harm to the person or to another person
  3. The immediate treatment will be provided to the person if the person is subject to a temporary treatment order
  4. There is no less restrictive means reasonably available to enable the person to receive the immediate treatment.
76
Q

What things would you consider in the risk assessment of an older adult with dementia?

A

MONEY can’t buy MEDALS or the independence of DRIVING

Money – Finances, can they pay bills, manage their money?

M – Mobility and falls assessment

E – Eating, can they buy food, cook it and eat it?

D – Danger – leave oven on, forget to turn on the cold water?

A – Aggressive when they get confused or hallucinate?

L – Lost (walking, supermarket, disoriented within home)

S – Sexual disinhibition?

Driving – Driving okay? Check whether they remember the road rules, get lost or confused

77
Q
A

Year 4C - psych (3 decks)

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