Psychiatry Flashcards
What is Alzheimer’s disease
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
What is the epidemilogy of Alzheimer’s disease
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
What is the aetiology of Alzheimer’s disease
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
How does Alzheimer’s disease present
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
How is potential Alzheimer’s disese assessed
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
What are the diagnositic findings in Alzheimer’s dementia
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)
How is Alzheimer’s managed
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
How is alzheimer’s disease treated
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)
What is the prognosis in Alzheimer’s dementia
Mean survival time is ~3 to 10 years after diagnosis
What are potential complications of Alzheimer’s dementia
Infections: aspiration pneumonia most common contriputing factor to AD-related mortality
Malnourishment/ dehydration
Intracerebral hameorrhage (↑ risk due to cerebral amyloid angiopathy)
What is vascular dementia
Gradual cognitive decline caused by small or large vessel disease
What is the epidemiology of vascualr dementia
Second most common type of dementia (15-20%)
Prevalenc eincreases with age
What is the aetiology of vascular dementia
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
What are the risk factors for vascular dementia
Advanced age History of stroke Underlying conditions associated with cardiovascular disease: - chronic hypertension - hyperglycaemia - hypercholesterolemia - hypertriglyceridemia - obesity
How does vascular dementia present
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
How is vascular dementia diagnosed
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
How is vascular dementia treated
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
What is Lewy Body dementia
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
What is the epidemiology of Lewy body dementia
Second most common form of neurodegnerative dementia 10-20% of dementia cases
Male > Female (4:1)
How does lewy body dementia present
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
How is lewy body dementia diagnosed
MRI showing atrophy of substantia innominata and mesopontine grey matter
How is lewy body dementia treated
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
What is the prognosis of lewy body dementia
Median survival of ~10 years
What is schizophrenia
A sever psychiatric disorder characterised by chronic or recurrent psychosis
What is the epidemiology of schizophrenia
Prevalence: < 1% Sex: ♂ > ♀ (∼1.4:1) Age of onset: late teens to mid-30s Men: typically early 20s Women: typically late 20s
What is the aetiology of schizophrenia
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
What are the risk factors for schizophrenia
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
How does schizophrenia present
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)
What are the positive symptoms of psychosis
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
What are the types and subtypes of delusions
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
What are the types of disorganised thought and speech processes
- 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
What are the negative symptoms of psychosis
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
What are the abnormal motor behaviours which may be present in schizophrenia
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
What are the cognitive symptoms of schizophrenia
Inattention
Impaired memory
Poor executive functioning
What are the mood symptoms of schizophrenia
Anxiety Depression Social or specific phobia PTSD OCD Panic disorder
How is schizophrenia diagnosed
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
How is schizophrenia treated
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
What is the prognosis of schizophrenia
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)
What is schizoaffective disorder
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.
What are the types of schizoaffective disorder
Manic - psychotic and manic symptoms
Depressive - psychotic and depressive symptoms
Mixed - psychotic and both manic and depressive symptoms
