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Year 4 > Psychiatry > Flashcards

Psychiatry Flashcards

1
Q

What is Alzheimer’s disease

A

A neurodegnerative syndrome with progressive decline in several cognitive domains

Atrophy of the cerebral cortex and formation of amyloid plaques and neurofibrillary tangles and acetylcholone production in affected neurones is reduced

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2
Q

What is the epidemilogy of Alzheimer’s disease

A

50-75% of dementia cases
800,000 people in the UK have dementia
Prevalence of dementia increases with age with 20% of people over 80 known, although ~half of likely cases have actually been diagnosed
Similar prevalence in men and women

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3
Q

What is the aetiology of Alzheimer’s disease

A

Formation of beta amyloid plaques and neurofibrillary tangles
Neuronal loss is selective - the hippocampus, amygdala, temporal neocortec and subcortical nuclei
Cerebral atrophy (medial temporal lobe), senile plaques, amylpid deposition, neuro-fibrillary tangles, acetyle choline levels reduced
95% of AD pts show evidenc of VD too

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4
Q

How does Alzheimer’s disease present

A

5 A’s of Alzheimers:
Amnesia - memory loss (short term goes first)
Aphasia - inability to speak, write or understand language both written and verbal
Agnosia - inability to recognise sensory stimuli
Apraxia - inabiltiy to perform learned movements on command
Associated behaviours - disorientation, misplacing items, decline in activities of daily living, personality changes

Mood changes - depressed, apathetic, irritable
Poor abstract thinking - complex tasks requiring organisation and planning become difficult
Construction dyspraxia - parietal lobe deficits may lead to difficulties completing clock-drawing test

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5
Q

How is potential Alzheimer’s disese assessed

A

Use neuropsychological testing (mini-mental state exam, Montreal cognitive assessment) in those with memory loss, cognitive and/or functional decline

Rule out organic causes:

  • medication review
  • lab tests for hypothyroidism and B12 deficiency
  • Neuroimaging to rule out VD, hydrocephalus, tumors)
  • Clinical assesment of depression to rule out psuedodementia

AD can only be confirmed via neurohistopathological examination, which can only be conducted post mortem

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6
Q

What are the diagnositic findings in Alzheimer’s dementia

A 
Insidious onset (often first noticed by relatives)
Objectively confirmed progressive loss of function in at least two cognitive domains (usually including memory impairment)
Impaired activities of daily living
No other plausible explanation (eg delirium)
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7
Q

How is Alzheimer’s managed

A

Repeated cognitive testing used to track disease progression
Functional testing

EEG - slower basic rhythm, evoked potentials with long latency

Neuroimaging:
CT/ MRI
- signs of generalised focal cerebral atrophy
- enlarged ventricles
-narrowing of gyri
- prominent cerbral sulci
-Disproportionate atrophy of the hippocampus and/or medial temporal lobe

Cerbrospinal fluid:

  • ↑ Phospho-tau protein
  • ↓ β-amyloid proteins Aβ1–42
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8
Q

How is alzheimer’s disease treated

A

Pharmacological treatment:

Mild to moderate:

  • acetylcholinesterase inhibitors:
    • Donepezil
    • Galantamine
    • Rivastigmine

Moderate to severe:

  • in addition to acetylcholinesterase inhibitors, give NMDA-receptor antagonist:
    • Memantine

Associated aggression and psychosis:

  • low dose antipsychotics:
    • atypical eg risperidone
  • SSRIs eg citalopram in those with depression

Non-pharmacological Treatment:

Lifestyle modification:

  • regular sleep schedule
  • familiar environment
  • remove ambient noise

Cognitive rehabilitiation:
- memory training (eg puzzles, interactive games) to support memory retention and strategies to compensate for cognitive and functional decline

Physical activity:
-improves physical strength which slows functional decline

Avoid drugs with strong anticholinergic effects (eg diphenhydramine)

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9
Q

What is the prognosis in Alzheimer’s dementia

A

Mean survival time is ~3 to 10 years after diagnosis

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10
Q

What are potential complications of Alzheimer’s dementia

A

Infections: aspiration pneumonia most common contriputing factor to AD-related mortality
Malnourishment/ dehydration
Intracerebral hameorrhage (↑ risk due to cerebral amyloid angiopathy)

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11
Q

What is vascular dementia

A

Gradual cognitive decline caused by small or large vessel disease

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12
Q

What is the epidemiology of vascualr dementia

A

Second most common type of dementia (15-20%)

Prevalenc eincreases with age

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13
Q

What is the aetiology of vascular dementia

A

Occurs as a result of a prolonged or severe cerebral ischaemia of any aetiology primarily:

  • Large artery occlusion (usually cortical ischaemia)
  • Lacunar stroke (small vessel occlusion resulting in subcortical ischaemia)
  • Chronic subcortical ischaemia
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14
Q

What are the risk factors for vascular dementia

A 
Advanced age
History of stroke
Underlying conditions associated with cardiovascular disease:
- chronic hypertension
- hyperglycaemia
- hypercholesterolemia
- hypertriglyceridemia
- obesity
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15
Q

How does vascular dementia present

A

Symptoms depend on location of ischaemic events and so vary widely between pts

Small vessel:

  • progress gradually or stepwise and slower than in multi-infarct dementia
  • signs of subcortical pathology:
    • Early symptoms
  • – Reduced executive functioning
  • – Loss of visuospatial abilities
  • – Confusion
  • – Apathy
  • – Motor disorders (gait disturbance, urinary incontinence
    • Later symptoms
  • – Impaired memory
  • – Further cognitive decline - loss of judgement, disorientation
  • – Mood disorders - euphoria, depression
  • – Behavioural changes - aggression
    • Advanced stages
  • – Further motor deteriation - dysphasia, dysarthria

Large vessel:

  • usually sudden onset
  • multi-infarct dementia
  • typically stepwise deterioration
  • signs of cortical pathology
    • cognitive impairment in combination with asymmetric or focal deficits (eg unilateral visual field defects, hemiparesis, present Babinski reflex
  • symptoms depend on affected cerebral region
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16
Q

How is vascular dementia diagnosed

A

Clinical diagnosis based on medical history, clinical features, MMSE testing and supported by imaging findings

Brain MRI: multiple cortical infarcts, subcortical infarcts (lacunes) and white matter lesions (periventricular and in the semioval centre)

Brain CT: microangiopathic lesions located in white matter, multiple lacunar lesion in the subcortical brain regions

PET-CT (functional imaging): may br helpful in distinguishing between AD and VD:

  • VD- hypoperfusion and hypometabolism more pronounced in the frontal lobe
  • AD- hypoperfusion and hypometabolism more pronounced in the patietal and temporal lobes

Ultrasound:

  • Doppler exam of crital vessels (particularly the carotid arteries) for signs of cerebrovascular risk (atherosclerosis)
  • Echocardiogram to evaluate the risk of cardioembolic events

Lab tests:
-GLucose
-TSH
To rule out other potential causes or comorbidities

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17
Q

How is vascular dementia treated

A

VD results in an irreversible loss of cognitive skills
Management is aimed at symptom control and prevention of addition ischaemic events

Memory training:

  • practicing image recognition
  • completing arithmetic or combinatorial problems
  • recalling past memories

Eliminate individual risk factors (antihypertensive therapy, treatment of diabetes, weight reduction)

Consider antiplatelet drugs (must assess bleeding risk)

Adjuvant treatment

  • SSRIs
  • GI tube for feeding
  • Sleep hygiene
  • Pain management
  • Benzodiazepines in anxiety management
  • Physical exercise
  • Familiar routine and environment
  • Music therapy and animal assisted therapy

Avoid anticholinergic substances (eg tricyclic antidepressants) as may lead to further cognitive decline

18
Q

What is Lewy Body dementia

A

Onset of both cognitive and motor symptoms within one year of each other
Fluctuating cognitive impairment, detailed visual hallucination and Parkinsonism
Lewybodies in brainstem and neocortex

19
Q

What is the epidemiology of Lewy body dementia

A

Second most common form of neurodegnerative dementia 10-20% of dementia cases
Male > Female (4:1)

20
Q

How does lewy body dementia present

A

Sequence of symptoms is more variable than in other types of dementia

Impairments in memory, speech, reasoning, intellectual function, and/or spatiotemporal awareness

Bradykinesia, rigidity, dystonia, athetosis, chorea, ballismus, akathisia, tics, and tremors

Visual hallucination and paranoid episodes

↑ Sensitivity to neuroleptic medication and metabolic perturbation

Episodic impairment of cognition or vigilance

Rapid eye movement sleep behaviour disorder

Frequent falls

21
Q

How is lewy body dementia diagnosed

A

MRI showing atrophy of substantia innominata and mesopontine grey matter

22
Q

How is lewy body dementia treated

A 
No curative therapy
Symptomatic treatment:
-supportive therapy
-behavioral therapy
-physical therapy
-pharmacotherapy
-- parkinsonian symptoms - treat like Parkinson disease
-- dementia symptoms -treat with:
--- acetylcholinesterase inhibitors (donepezil)
--- Memantine
--- Adjuvant treatment of symptoms
23
Q

What is the prognosis of lewy body dementia

A

Median survival of ~10 years

24
Q

What is schizophrenia

A

A sever psychiatric disorder characterised by chronic or recurrent psychosis

25
Q

What is the epidemiology of schizophrenia

A 
Prevalence: < 1%
Sex: ♂ > ♀ (∼1.4:1)
Age of onset: late teens to mid-30s
Men: typically early 20s
Women: typically late 20s
26
Q

What is the aetiology of schizophrenia

A

Exact mechanism is unknown but is thought to relate to increased dopaminergic activity in the mesolimbic neuronal pathway and decreased dopaminergic activity in the prefrontal cortical pathway

27
Q

What are the risk factors for schizophrenia

A

Genetic factors : risk significantly increased if relatives also affected

  • One schizophrenic parent ~10%
  • Two schizophrenic parents ~40%
  • Concordance rate in identical twins ~30-40%
  • Concordance in fraternal twins ~10-15%

Environmental factors:

  • stress and psychosocial factors
  • frequent use of cannabis during early teens (increased incidence and worse course of positive symptoms)
  • urban environment
  • advanced paternal age at conception
28
Q

How does schizophrenia present

A

A prodrome of negative symptoms and psychosis that precedes the positive psychotic symptoms
May also have associated abnormal motor behaviours, cognitive symptoms, mood symptoms, anxiety, neurological abnormalities (sensory disturbance and impaired coordination), and/or metabolic abnormalities (hypertension, diabetes, hyperlipidemia)

29
Q

What are the positive symptoms of psychosis

A 
Hallucinations - perpetual abnormalities in which sensory experiences occur in the absence of external stimuli
Illusions - a perpetual abnormality, in which real external stimuli are misinterpreted
Hallucinations and illusions can be:
-Auditory (most common)
-Visual
-Somatic (tactile)
-Gustatory
-Olfactory

Delusions - fixed false beliefs that are maintained despite being contradicted by rality or rational arguments and are not related to one’s religious beliefs or culture

Disorganised thought and speech processes

30
Q

What are the types and subtypes of delusions

A

Types:

  • Bizarre- delusions that cannot be true or are inconsitent with the patient’s social and cultural norms
  • Nonbizzare- delusions that can be true or are consistent with the patients’s social and/or cultural norms

Subtypes:

  • Grandiosity- the patient insists they have special powers or importance
  • Ideas of reference- believes that normal events are of special importance to them (eg tv reporter is talking about them)
  • Paranoia- an exaggerated distrust of others and suspicion of their motives
  • Persecutory- believes they are being cheated on, conspired against or harassed
  • Erotomania- believes otehrs are in love with them
  • Jealousy- believes their partner is unfaithful without justification
  • Somatic delusion - believes they are experiencing a bodily function or sensation when there is none present
  • Mixed delusions- two or more delusions occuring simultaneously with neither predominant over the other
  • Unspecified delusions- one which does not fit the criteria of other types or connot be clearly defined
31
Q

What are the types of disorganised thought and speech processes

A
  • Loose associations: incoherent thinking expressed as illogical, sudden and frequent topic changes
  • Word salad: incoherent thinking expressed as a sequence of words without a logical connection
  • Tangential speech: nonlinear thought expressed as a gradual deviation from the focused idea or question
  • Neologisms: the creation of new wrods with peculiar meanings
  • Echolalia: involunary repitition of other’s words or sentences
  • Flight of ideas: quick succession of thoughts usually demonstrated in a continuous flow of rapid speech and abrupt changes in topic
  • Clang associations: use of words based on rhyme patterns rather than meaning
  • Circumstantial speech: nonlinear thought expressed as a longwinded manner of explanation with multiple devisions from the central topic, before finally expressing the central idea
  • Thought blocking: an objective observation of an abrupt ending in a thought process, expressed as a sudden interruption in speech
  • Pressured speech: accelerated thoughts that are expressed as rapid, loud and voluminous speech, often in the absence of social stimulation
32
Q

What are the negative symptoms of psychosis

A

Flat affect- reduced or absent emotional expression
Avolition- reduced or absent ability to initiate purposeful activities
Alogia- impaired thinking that manifests with reduced speech output or poverty of speech (eg one word answers)
Anhedonia- inability to feel pleasure from activities which were previously enjoyable or form any new positive stimuli
Apathy- lack of emotion or concern, especially with regard to matters that are normally considered important
Emotional and social withdrawl

33
Q

What are the abnormal motor behaviours which may be present in schizophrenia

A

Grossly disorganised behaviour - an abnormal behaviour characterised by inadequate goal-directed activity (purposeless movements) and bizarre emotional responses (eg smiling or laughing when inappropriate)

Catatonia- A state of abnormal behavior and movement, often including catalepsy (immobility), purposeless motor activity, strange postures, negativism, and mutism

34
Q

What are the cognitive symptoms of schizophrenia

A

Inattention
Impaired memory
Poor executive functioning

35
Q

What are the mood symptoms of schizophrenia

A 
Anxiety
Depression
Social or specific phobia
PTSD
OCD
Panic disorder
36
Q

How is schizophrenia diagnosed

A

Clinical diagnosis
At least two of:
-delusions
-hallucinations
-disorganised speech
-grossly disorganised or catatonic behaviour
-negative symptoms
Which must persist for >1 months over a period of continuous disturbance for >6 months
Must cause social, occupational or personal functional impairment lasting >6months
Rule out schizoaffective or mood disorder with psychotic features
Medical or substance use disorder ruled out too

Brain imaging often shows cortical atrophy, decreased hippocampal and temporal massa dn enlargemnt of the cerebral ventricles

Rule out medical or substance use disorder by:

  • urine toxicology
  • blood tests eg FBC, metabolic panel, LFTs, TSH and fasting glucose
  • ECG to assess:
    • presence or absence of metabolic syndrome
    • baseline QTc interval before starting antipsychotics
37
Q

How is schizophrenia treated

A

Estabilsh therapeutic alliance
Acknowledge emotional state
Avoid validation of delusions or confronting delusional nature of symptoms
Initial response to treatment within the first 2-4 weeks is associated with a better long term response
Hospitalisation is acutely psychotic

Pharmacotherapy:

Acute psychotic episode - short acting antipsychotics
Acute manic episode - mood stabilizers (eg lithium, valproate, carbamazepine)

First line: second generation (atypical) antipsychotics (eg risperidone, quetiapine) which are especially effective at treating positive psychotic symptoms
Alternative: first generation (typical) antipsychotics

Treatment non adherence: use long-acting injectable formulations

  • first gen: fluphenazine, haloperidol
  • second gen: risperidone, aripiprazole, olanzapine, paliperidone

Treatment resistense schizophrenia (persistent positive symptoms despite trials >6weeks of 2 different antipsychotics at their maximum doses:
-drug of choice - clozapine -requires regular FBC because of risk of agranulocytosis

Treatment during pregnancy:
-first gen: haloperidol

Treatment of associated depression:

  • SSRIs
  • Tricyclic antidepressants

Treatment of associated anxiety:
-SSRIs

Psychoeducation:
used as an adjunct to avoid relapse
-patient, fmaily and group psychosocial therapy and education
-cognitive behavioural therapy
-supportive social measures
38
Q

What is the prognosis of schizophrenia

A

It is a progressive disorder that causes significant impairment, with many patients presenting with psychosocial dysfunction

Predictive factors for an unfavourable course of illness:

  • Family history
  • Earlier onset of disease
  • Poor network of social support
  • Male
  • Slower onset of illness
  • More negative symptoms
  • Depression
  • Concomitant substance use disorder
  • Suicidal ideation/ suicide attempt

Patients with schizophrenia are at an increased risk for alcohol use disorder, depression, violence, and suiced (~5% complete suicide)

39
Q

What is schizoaffective disorder

A

A condition where symptoms of both psychotic and mood disorders are present together during one episode or within a two week period of each other

Characterised by persistent mood disorder symptoms with episodic psychotic symptoms for at least 2 weeks at a time.

40
Q

What are the types of schizoaffective disorder

A

Manic - psychotic and manic symptoms
Depressive - psychotic and depressive symptoms
Mixed - psychotic and both manic and depressive symptoms

Year 4 (6 decks)

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