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Phase 3a Medicine > Psychiatry > Flashcards

Psychiatry Flashcards

1
Q

Definition of Delirium

A

Acute confusional state with with altered mental status.

Acutely fluctuates with:
1. inattention
2. disorganised thinking
3. altered consciousness

due to underlying cause

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2
Q

Screening tool for delirium

A

DSM-V

ALL 4 OF THE FOLLOWING NEED TO BE PRESENT:

  1. Acute Development - hrs to few days - fluctuating
  2. disturbed cognition - not accounted for by pre-existing dementia.
  3. Disturbed attention and awareness - reduced orientation
  4. occurs due to physiological consequence of a physical condition, substance intoxication or substance withdrawal.
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3
Q

Risk Factors and Causes of Delirium

A

old age - over 65
long hospital stay/care
home stay
hip fracture
acute illness

dementia - dementia and delirium can both cause each other.

psychological agitation - due to being in pain

previous cognitive impairement

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4
Q

Underlying Aetiology of Delirium

A

CHIMPS PHONED V

C - constipation
H - hypoxia
I - infection - uti,pneumonia - even malaria, wound ix or intracranial infection
M - metabolic disorder - liver/renal failure, hypo/hyper natremia , hypo/hyper glycaemia, anaemia
P - post operative or post general anesthesia
S - sleeplessness

P - pain
H - hypothermia/ pyrexia
O - organ dysfunction
N - nutrition - b12 def, thiamine def, nicotinic acid def
E - environmental changed
D - drugs or drug withdrawal

V - VASCULAR - stroke or mi

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5
Q

Classifications of Delerium

A

Hypoactive - lethargic, slow, incoherent speech, withdrawn

hyperactive - restless, agitated, aggressive, hallucinated, aroused

mixed - mix of both

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6
Q

Investigations of Delirium

A

Clinical Diagnosis

  1. patient hx - figure out baseline cognitive status
  2. medication review
  3. systems review
  4. screening tools : dsm-v, cam , cam-icu, amts

cam - confusion assessment method

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7
Q

Questions you would ask for AMTS

A
  1. AGE
  2. DOB
  3. TIME
  4. RANDOM ADRESS REPEAT - AND AT END
  5. WW1 YR?
  6. LOCATION? HOUSE NO?
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7
Q

Additional Ix for Delirium

A

Bloods - fbc,lft,tft,glucose, u+E, ABG

Urinalysis

Imaging - CXR/CT HEAD - FOR HEAD/LUNG PATHOLOGY

ECG - exclude MI

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8
Q

Management

A

Treat underlying condition

supportive
1. reorientation - inform pt of who they are, where they are and what happened
2. family+ friends visit
3. fluid balance monitor - look for constipation

medical:

  1. halloperidol - if at risk of harming themselves or others
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9
Q

Differentials of Delirium

A
  1. dementia
  2. epilepsy
  3. underlying cause - CHIMPS PHONED V
  4. ANXIETY
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10
Q

Delirium vs Dementia

A

Some factors in favour of delirium :

  1. impaired consciousness
  2. fluctuating symptoms - worse at night, normal at times
  3. abnormal perception
  4. agitation and fear
  5. delusion
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11
Q

Define Dementia

A

Syndrome of deterioration in cognition that results in impairment in activities of daily living.

chronic/progressive

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12
Q

What higher cortical functions does dementia affect?

A

thinking
memory
language
comprehension
orientation

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13
Q

2 types of memory dementia affects

A

semantic - explicit memory like remembering names, words, facts, events

implicit - non declarative memory. - memory that doesn’t require conscious recollection. - eg learned tasks, skills.

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14
Q

Causes of Dementia

A

Most causes chronic and progressive in nature.

  1. alzheimers
  2. lewy body
  3. vascular
  4. huntingtons
  5. frontotemporal atrophy
  6. normal pressure hydrocephalus
  7. Creutzfeld- jakob disease

others:
1. neoplastic
2. trauma - haemorrhage, haematoma
3. infection - lyme disease, neurosyphilis, tuberculosis meningitis, HIV
4. drugs - barbiturates, alcohol
5. endocrinological - cushings, vitamin b12 def, thyroid disease
6. psychiatric - delirium/dementia

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15
Q

Define Alzheimer Disease

A

Chronic progressive neurodegenerative disorder characterised by brain lesions of neurofibrillary tangles, amyloid plaques, neuronal loss, Ach synthesis dysfunction.

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16
Q

deteriorating course of alzheimers

A

8-10 years

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17
Q

Presentation of Alzheimers

A

gradual onset

4A’S
AMNESIA - recent memory first lost. difficult learning new information
AGNOSIA - problems with recognition using the senses of hearing, smell, taste, touch, vision. For example, an inability to recognise the smell of a food or the feeling of a full bladder.
APHASIA - difficulty finding the correct words, muddled speech, disjointed conversations.
APRAXIA - inability to carry out skilled tasks despite normal motor function.

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18
Q

Pathological Changes seen for Alzheimers

A

Macroscopic - Cerebral Atrophy involving cortex and hippocampus.

microscopic - cortical plaques due to AB amyloid protein and neurofibrillary tangles.
tau hyperphosphorylation.

Biochemical - Acetylcholine deficiency

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19
Q

Risk Factors of Alzheimers

A

increased age
downs
caucasian
Fhx
Genetics

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20
Q

Pathophysiology of Alzheimers

A

Normally a-secretase and y-secretase cleave APP to form soluble peptide.
In Alzheimers you have b-secretase and y-secretase cleavage = AB monomer = insoluble
AB42 ISOFORM = hydrophobic , prone to aggregate and oligomerise.

cause kinase activation - tau hyperphosphorylation.

hyperphosphorylated tau proteins aggregate to form neurofibrillary tangles.

ab42 oligomers then form fibrils and then amyloid plaques.

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21
Q

what is tau

A

protein that stabilises microtubules

so with hyperphosphorylation you get microtubule dysassembly, cell death and synaptic dysfunction.

NEURONAL DAMAGE

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22
Q

Genetic RF of Alzheimers

A

APP - codes amyloid precursor protein

PSEN1 - codes for presinilin 1

PSEN2 - codes for psen 2

ApoE - codes apolipoprotein E which is a cholestrol transport protein.

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23
Q

Investigations of Alzheimers

A

Bloods - fbc,esr,crp,u+e, lft,tft,b12,folate,hba1c

Assessments:
1. initial hx - from person and close person - ADL’s and Qol

  1. physical exam , neuro exam, focal neuro signs (coordination and gait, peripheral neuropathy, tremor, bradykinesia, rigidity) , visual/audio deficit, cvs (hypertension, arrhythmias, PVD)

Cognitive Assessment: screener and impairement test

  1. 10-CS - 3 temporal orientation qus (yr,month,date) and 3 word recall (4 point scaled animal naming task)
  2. 6-CIT - temporal orientation, address memory, count back from 20 , months in reverse.
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24
Q

Management of Alzheimers

A

Non- med - group cognitive stimulation. cognitive rehab, group reminiscence therapy

Medical:

Acetylcholinesterase inhibitors- increase neuronal excitation by increases nAChR activity.

  1. donepezil - CI in bradycardic pts. - insomnia possible
  2. galantamine
  3. rivastigmine

memantine - weak NMDA antagonist. NMDA is excitatory but chronic weak NMDA activity is pathological. so you inhibit weak activity, boost strong activity and you have better cognitive function.

memantine if AchE inhibitors CI’d or as add on for severe alzheimers.

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25
Q

Define Lewy Body Dementia

A

progressive neurodegenerative disorder.

lewy body deposition in substantia nigra, paralimbic and neocortical areas.

Lewy bodies are cytoplasmic inclusions of alpha-synuclein.

with impairment to mitochondrial function you get misfolding and aggregation of alpha synuclein.

26
Q

what is alpha synuclein

A

lipid binding protein within synaptic terminals that regulate synaptic vesicle trafficking and recycline.

27
Q

Investigations of lewy body dementia

A

clinic diagnosis

single - photon emission CT - SPECT . - called a DaTscan = measures uptake of dopaminergic iodine.

90% sensitivity and 100% specificity.

28
Q

presentation of lewy body dementia

A
  1. visual hallucinations
  2. parkinsonism - develops after cognitive impairment. its a motor syndrome that has bradykinesia, pill-rolling tremor, lead pipe rigidity and instability.
  3. fluctuating cognition - lose attention and executive function early comparative to mess loss in Alzheimers.

FLUCTUATES RATHER THAN DECLINE AS EVERY OTHER DEMENTIA. it is however progressively declining.

29
Q

Medical Mx of Lewy Body Dementia

A

acetylcholinesterase inhibitor - donepezil, rivastigmine, galantamine) and memantine.

neuroleptics (antipsychotics) are AVOIDED - can cause irreversible parkinsonism in LWB pts as theyre very sensitive.

30
Q

Define Vascular Dementia

A

2nd most common.

group of syndromes of cognitive impairment caused by ischaemia or haemorrhage secondary to cerebrovascular disease.

vascular cognitive impairement is spectrum of disease caused by impaired blood flow to brain, and vascular dementia is most severe form of VCI.

31
Q

RF of Vascular Dementia

A

Vascular Disease
DM
SMOKING
OBESITY
CHD
HYPERLIPIDEMIA
HYPERTENSION
AF
STROKE - 9* HIGHER THAN GEN POP
MALE - INCREASED RISK OF VASCULAR DISEASE

32
Q

Classification of Vascular Dementia

A
  1. Stroke related - multiple-infarct or single infarct dementia
  2. subcortical - due to small vessel disease
  3. mixed - VD and Alzheimers
  4. inherited - cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) .
33
Q

Presentation of Vascular Dementia

A

Stepwise deterioration - period of stability followed by acute decline progression.

occurs over several months/years. - due to progressive infarcts over time.

mood disturbance.
focal neurological abnormalities - motor, sensory, or visual symptoms for example.
impaired concentration
seizures
memory disturbances
gait disturbance
speech disturbance
psychosis, hallucination, delusion - in later disease

34
Q

Investigations of Vascular Dementia

A

NINDS-AIREN criteria.

  1. presence of cognitive decline interfering with ADLs - clinical exam and cognitive assessment.
  2. presence of cerebrovascular disease. - MRI and/or neuro signs (facial paralysis, ataxia, visual field defect, motor weakness, aphasia, dysarthria)
  3. relationship between cognitive decline and cerebrovascular disease
    - onset of dementia less than 3 months after stroke
    - abrupt deterioration in cognitive function
    - stepwise progressive of cognitive decline
35
Q

Management of Vascular Dementia

A

treat underlying vascular rf to slow progression.
symptomatic tx also provided to provide support to patient and carers.

non pharm tx:

  1. cognitive stimulation
  2. multi-sensory stimulation
  3. music and art therapy
  4. animal assisted therapy.

NO PHARMACOLOGICAL TX unless comorbidity with alzheimers, parkinsons, dlb.

36
Q

Define Frontotemporal dementia

A

Atrophy of frontal and temporal lobes. 3rd most common.

unknown aetiology.

fhx - rf and genes.

frontal and temporal lobe neuronal death due to protein dep. - tau proteins

37
Q

subtypes of frontotemporal dementia

A

picks disease
progressive non-fluent aphasia**/chronic progressive aphasia
semantic dementia

(struggle to get words out and speak in short sentences)

38
Q

presentation of frontotemporal dementia

A

onset before 65
personality changes and social conduct issues early on
gradual onset
preserved memory and visuospatial skills

39
Q

picks disease definition

A

caused by tau aggregation in neurones - only diagnoses post mortem.

these tau proteins are diff to alzheimers as they stain differently - SILVER STAIN.

40
Q

staining of pick bodies

A

tau aggregates - SILVER STAINING (microscopic)

41
Q

how is picks disease characterised

A

behavioural changes

  1. personality changes
  2. impaired social conduct
  3. hyperorality - compulsive need to place objects in ones mouth.
  4. disinhibition.
  5. increased apetite
  6. perseveration behaviours - uncontrolled repetition of action, word, thought, activity, emotion.
42
Q

in picks disease how does the chronic progressive aphasia present?

A

speech changes mostly

  1. speech apraxia - poor articulation
  2. effortful and non-fluent speech
  3. comprehension is preserved relatively.
  4. progressive breakdown in language output.
43
Q

in picks disease how is semantic memory affected?

A

changes in meaning in language or logic:

  1. fluent speech but is empty and conveys little meaning.
  2. decline in understanding in meaning of words.
  3. inability to retrieve names
  4. inability to recognise objects and familiar faces (prosopagnosia)
44
Q

Mx of Picks Disease

A

NOTHING

45
Q

Define Normal Pressure hydrocephalus

A

Reversible cause of dementia.

elderly

due to impaired absorption of CSF by arachnoid villi.

can happen secondary to head trauma, subarachnoid haemorrhage or meningitis.

46
Q

presentation of normal pressure hydrocephalus

A

wet - urinary incontinence
wobbly - gait abnormality - similar to parkinsons
wierd - dementia or bradyphrenia - slowed thinking and processing of info.

47
Q

ix of normal pressure hydrocephalus

A

MRI - to see anatomical differences.

you might see hydrocephalus with ventriculomegaly without widening sulcus between ventricles.

48
Q

Mx of normal pressure hydrocephalus

A

Ventriculoperitoneal shunt - helps drain fluid from brain into peritoneal cavity.

49
Q

Creutzfeldt-jakob disease def

A

rapidly progressive condition

occurs due to prion proteins.

these proteins occur due to misfolding in which we have beta-pleated sheets resistant to proteases.

VERY RARE.

50
Q

presentation of creutzfeldt-jakob disease

A

rapid onset dementia
myoclonus - brief, involuntary twitching of muscle groups

51
Q

Dementia vs Depression

A

things that favour depression over dementia :

rapid onset with short history
biological sx like weight loss, low mood, sleep disturbance
pt aware of memory loss

global memory loss - pseudodementia - lose all memory. dementia is recent memory loss usually.

52
Q

Characteristics of Depression

A

-persistent low mood
- loss of interest and enjoyment in daily activities (anhedonia)
- neurovegetative disturbances - . so like apetite, sleep and concentration disturbance.
- social and occupational disturbance
- suicidal ideation

53
Q

depression in adults - define

A

clinical syndrome - involving mood cognition and behaviour.

can be reactive (stress no hereditary) or endogenous (hereditary no circumstantial)

54
Q

aetiology of depression

A

not well undertood.

genetics have strong links but no specifics?

stressful life events,personality, sex.

55
Q

rf of depression

A

postnatal status
fhx
dementia
corticosteroid use
stress
propranolol
oral contraceptive
co-existing medical conditions
female - women double chances

substance misuse
stressful life events
obesity

56
Q

Pathophysiology of depression

A

Abnormal concentrations of neurotransmitters, dysregulation of HPA axis, and secondary messenger abnormalities.

3 main biological theories:

  1. monoamine theory - impaired monoamine signalling to certain regions in brain.
  2. neuroendocrine theory -
  3. trophic/ neuroplastic theory -
57
Q

what diseases can lead to depression

A

neuro: Parkinson’s, dementia, multiple sclerosis
endo: hypothyroid, Cushing’s, Addison’s
cancers
drugs - alcohol, propranolol, benzodiazepines, methyldopa

58
Q

presentation of depression

A

low mood and anhedonia most the day nearly every day.

possible functional impairment in social and occupational situations.

59
Q

criteria for depression

A

DSM-V - if 5/9 are seen and present nearly every day for over 2 weeks then make a diagnosis.
at least 1 of them need to be depressed mood or anhedonia.

  1. depressed mood
  2. anhedonia
  3. weight changes - either way, change in appetite
  4. sleep disturbance - either way insomnia/hypersomnia
  5. psychomotor agitation or retardation - restless, anxious leading to repetitive, unintentional movement.
  6. fatigue
  7. excessive guilt - worthless feeling
  8. poor concentration
  9. suicidal ideation
60
Q

additional criteria for depression

A

sx must cause significant distress or functional impairment.

episode cant be due to physiological effects of substance or other medical condition.

no hx of manic or hypomanic episodes.

episode not better explained by something else.

61
Q

classification of depression

A

PHQ-9 - tells you if less or more severe

less is less than 16.
more is 16 or more.

screening is PHQ-2.

62
Q

Management of Depression

A

less severe dep: least intrusive first

self-help, cbt, group exercise, mindfulness, meditation, IPT, SSRI’s, counselling

more severe:
1. cbt and antidepressant
2. cbt
3. counselling
4. short term psychodynamic psychotherapy
5. self help or group exercise

63
Q

examples of antidepressants

A

SSRI - Increase activity on post-synpatic 5-HT1a receptor to decrease depression

  1. citalopram
  2. escitalopram
  3. fluoxetine (1st line in kids)
  4. paroxetine
  5. sertraline

SNRI

Phase 3a Medicine (16 decks)

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