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2nd Year - Systems 3 > Neuro 5 - dementia and coma > Flashcards

Neuro 5 - dementia and coma Flashcards

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1
Q

Types of mood disorder

A

Depression - monopolar
Mania - monopolar
Manic depression - bipolar - treated well with mood stablisers

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2
Q

Depression

A

Emotional symptoms - mood + thought disorder
Biological symptoms - anhedonia, motivational impairment
Cognitive symptoms - difficulty decision making, poor concentration
Psychotic symptoms

  • treatment focuses mainly on improving mood and motivational impairments
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3
Q

Mania + bipolar disorder

A
  • need less sleep
  • excessive exuberance, enthusiasm, confidence, grandiosity
  • increased libido
  • behaviours inappropriate to circumstances
  • disorders of thought (psychosis)

May need different drugs for both manic and depressive episodes (and psychosis)
Also preventative medication, mood stabilisers (lithium, anti-epileptic drugs, atypical antipsychotics)

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4
Q

Causes of depression

A

CHEMICAL IMBALANCE - monoamine theory, well supported BUT delayed onset action antidepressants?
- functional deficit in 5-HT (serotonin) and/or noradrenaline/dopamine

NEURODEGENERATION
- neural apoptosis and neurogenesis

IMMUNE RESPONSE
- sickness behaviour

GENES

ENVIRONMENT (stress)

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5
Q

Treatments for depression

A

Pharmacological
- enhance monoamine levels in CNS - monoamine reuptake inhibitors/monoamine oxidase inhibitors/pre-synaptic receptor antagonists
- specific receptor agonists or antagonists
(consider side effects! if therapy possible, do that)

Cognitive behavioural therapy (mild-moderate depression)

Neurological interventions (30% unresponsive to drugs)

  • electroconvulsive shock therapy
  • deep brain stimulation
  • vagal nerve stimulation
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6
Q

Typical antidepressants

A

(TCAs and specific reuptake inhibitors)

  • monoamine oxidase inhibitors (MAOI)
  • tricyclic antidepressants
  • SSRIs (selective serotonin reuptake inhibitors)
  • selective noradrenaline reuptake inhibitors
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7
Q

Monoamine oxidase inhibitors

A

MAOIs
eg IPRONIAZID, PHENELZINE, TRANYLCYPROMINE, MOCLOBEMIDE
- inhibits breakdown of monoamines (MAO found in all tissues inc GI tract)
Multiple side effects - ‘cheese reaction’, need low tyramine

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8
Q

Tricyclic antidepressants

A

eg AMITRIPTYLINE, DESIPRAMINE, CLOMIPRAMINE

  • block reuptake of monoamines (mainly NA and 5-HT)
  • many have active metabolites, issues
  • multiple side effects
  • cardiotoxicity, low therapeutic index!

Used less in depression now, often for pain management

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9
Q

Selective reuptake inhibitors

A

SSRIs - FLUOXETINE (= prozac)
+ SNRIs - REBOXETINE
- block reuptake of 5-HT/NA
- similar efficacy and time-course to TCAs
- lack cholinergic side effects - less weight gain, low toxicity in overdose, no food interaction, reduced drug interactions

BUT - still many side effects , specific to serotonin or noradrenaline related effects

Discontinuation syndrome esp in paroxetine, need to be weaned off gradually 6-8 weeks

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10
Q

Atypical antidepressants

A

Mixed action

VENLAFAXINE - SSRI at low doses, SNRI at higher
TRAZEDONE - SSRI + 5-HT2 antagonist
NEFAZODONE - SSRI + 5-HT2 antagonist
MIRTAZAPINE - NA and 5-HT antagonist
AGOMELATINE - melatonin agonist and 5-HT2 antagonist

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11
Q

Delayed onset of clinical efficacy of antidepressants

A

Increased synaptic monoamine concentration

  • > activation of somatodendritic autoreceptors - hippocampal neurogenesis
  • > receptor adaptation (plasticity) -> increased synaptic concentration - cognitive effects
  • > activation of pre-synaptic autoreceptors -> decreased neurotransmitter release - post-synaptic receptor adaptation

DON’T KNOW WHY, these are theories

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12
Q

Alternative applications for antidepressants

A

SSRIs
- all anxiety disorders - OCD, panic disorder, social phobia, anxiety disorders (esp depression associated), eating disorders

TCAs
- analgesia, migraine prophylaxis

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13
Q

Mood stabilising drugs

A

Lithium

  • mechanism unsure
  • effective in controlling mania
  • potential toxicity, carefully monitor

+ anticonvulsants - valproic acid, carbamezapine

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14
Q

Dementia definition

A
  • structurally caused
  • permanent or progressive
  • decline in several dimensions of intellectual function
  • interferes substantially with normal social or economical activity

May be static (often following single major injury) or progressive

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15
Q

Causes of dementia

A

Degenerative - Alzheimer’s, Parkinson’s, Huntingdon’s, MS, MND, Lewy body dementia etc

Vascular - multi-infarct dementia etc

Metabolic/endocrine - hypothyroidism, B12 deficiency

Infective - AIDS-dementia complex, Creutzfeld-Jacob disease etc

Post-neurological insult - open/closed head injury, anoxia, subarachnoid haemorrhage, CO poisoning

Toxic - alcohol, heavy metal, organic solvents

Space occupying lesion - chronic subdural haemorrhage, primary/secondary metastatic intracranial tumour

Other - normal pressure hydrocephalus, epilepsy, systemic lupus etc

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16
Q

Cortical vs subcortical dementia

A

SUBCORTICAL

  • mild-moderate severity
  • slow cognition
  • memory impairment
  • apathy, depression
  • extrapyramidal motor abnormalities
  • changes to striatum and thalamus

CORTICAL

  • more severe sooner
  • normal speed of cognition, but with frequent errors
  • more severe memory impairment, dysphasia, dyspraxia, agnosia
  • depression rarer
  • uncommon motor abnormalities
  • changes to cortical association areas
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17
Q

Features of Alzheimer’s disease

A

Neurodegeneration -> loss of cognitive function
4th leading cause of death in elderly, 30% of over 80year olds have

Post mortem shows
- general brain atrophy - shrinkage of cortex, narrowed gyri, widened sulcal margins
- extracellular plaques of β-amyloid (knotted shape)
- intracellular neurofibrillary tangles of tau protein as hyperphosphorylated by overactive kinases (teardrop shape)
(can only be diagnosed definitively on autopsy)

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18
Q

Symptoms of Alzheimer’s disease

A

MILD

  • confusion, memory loss
  • disorientation
  • problems with routine tasks
  • changes in personality and judgement

MODERATE

  • difficulty with ADL
  • anxiety, depression, paranoia, aggression, agitation, hallucinations
  • sleep disturbances
  • wandering, pacing
  • difficulty recognising family and friends

SEVERE

  • aphasia (understanding language)
  • apraxia (carrying out tasks)
  • agnosia (recognising things)
  • loss of speech
  • loss of appetite
  • loss of bladder and bowel control
  • > total dependence on caregiver
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19
Q

Amyloid-β plaques

A

In Alzheimer’s disease

  • amyloid precursor protein (APP) is cleaved by proteases, secretase alpha, beta and gamma
  • secretase alpha -> sAPP (secreted, good for cell, harmless growth factor)
  • secretase beta and gamma together -> Aβ protein, takes essential intracelullar part of APP
  • so altered balance between these enzymes -> amyloiogenesis

Aβ then aggregates, body can’t clear, forms amyloid plaques -> neuronal death

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20
Q

Risk factors for Alzheimer’s disease

A

Age - risk doubles each 10 years after 65
Family history - genes with mutations in APP?

+ possibles:

  • early traumatic head injury
  • female
  • lower educational level
  • high calorie/fat/cholesterol diet, low exercise
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21
Q

Creutzfeld-Jacob disease

Study These Flashcards
A

CJD

  • fatal, rapidly progressive dementia, loss of motor coordination
  • survival 6 months average
  • no clear gross pathological features
  • can be nvCJD, from contact with BSE infected beef, then long incubation period, forms abnormal form of prion protein, converts other proteins around it to this, aggregates
  • or spontaneous conformational change
22
Q

Currently licensed drug therapy for Alzheimer’s

Study These Flashcards
A

Cholinesterase inhibitors - increase ACh levels (cholinergic cells die early, attempt to compensate)
eg DONEPEZIL, GALANTAMINE, RIVASTIGMINE

Partial NMDA receptor antagonists - neuroprotective, reduce excitability
eg MEMANTINE

(no new licensed drug for 15 years)

23
Q

Potential targets for treatment of Alzheimer’s

Study These Flashcards
A

MODIFY Aβ PATHWAY

  • alpha/beta/gamma secretase inhibitors? to reduce Aβ formation
  • anti-aggregation agents? uses copper + zinc (highly charged) to pull other proteins in - effective but no cognitive effect
  • statins? link between high cholesterol and APP changes
  • enhance Aβ clearance? with immune therapy

MODIFY TAU PATHWAY (some dementias have only tau changes)

  • lithium?
  • microtubule modifiers?
  • tau aggregation inhibitors?
24
Q

Deontology

Study These Flashcards
A

Do your duty
- do not kill/lie/break confidences etc

(may create a corresponding right - right for patient to have doctor fulfil duty)

25
Consequentialism
Do that which has the best outcomes - greatest good for the greatest number = utilitarianism
26
Virtue ethics
Be virtuous | - person based, what would a virtuous person do?
27
Four ethical principles
Respect for autonomy - consent, self-rule Beneficence - provide benefit Non-maleficence - do no harm Justice - share resources fairly (Beauchamp and Childress)
28
Coma
Absent wakefulness, absent awareness - lasts more than 6 hours - cannot be awakened - fails to respond normally to painful stimuli, light, sound - lacks normal sleep-wake cycle - does not initiate voluntary actions
29
Vegetative state
Wakefulness, absent awareness - preserved capacity for spontaneous or stimulus-induced arousal - sleep-wake cycles present - reflexive and spontaneous behaviours - complete absence of behavioural evidence for self or environmental awareness ``` Continuing = 4 weeks + Permanent = 6/12 months + ``` = post-coma unresponsiveness? = unresponsive wakefulness syndrome? Better terminology
30
Advanced directives
Must not treat if competent adult refuses - or is assault/battery/trespass to patient ``` NEEDS - competence and - current refusal or - advance refusal (currently no capacity, but previous specific, written, witnessed refusal of life-support) ``` May not treat even if competent adult demands - right to refuse but not insist on treatment
31
Minimally conscious state
Wakefulness, minimal awareness - severely altered consciousness - minimal (but clearly discernible) behavioural evidence of self or environmental awareness demonstrated - inconsistent but reproducible responses above the level of spontaneous or reflexive behaviour - some degree of interaction with surroundings
32
Locked-in syndrome
Wakefulness, awareness (paralysed but conscious) - loss of all brainstem functions - absence of brainstem reflexes - pupillary, corneal, oculovestibular, cough - no spontaneous respiratory effort - will cease to maintain physiological function without ventilator support (may be kept on life-support to allow best interests decision-making (and organ donation))
33
Human tissue act 2004
- appropriate consent needed - for storage and use - of whole bodies, removal, storage and use of human material (organs, tissues, cells) - from deceased and living persons Consent given from - person (before death), eg organ donation, donate body to science - nominated representative, chosen by person before death - someone in qualifying relationship - spouse, parent/child, sibling, grandparent ect down list (though need general consensus) Act doesn't include hair, nails (cells outside body), non-identifiable DNA analysis, storage and use for research, existing collections
34
Delirium vs dementia
DELIRIUM - abrupt onset - fluctuating course - lasts hours-weeks - abnormal alertness (high or low) - disrupted sleep-wake cycle - impaired attention - delusional thought - incoherent speech - hallucinations and illusions DEMENTIA - insidious onset - slow-progression - lasts months-years - normal alertness - normal sleep-wake cycle - relatively normal attention - impoverished thought - word-finding difficulty in speech - intact perception early on
35
Neuropathology principles in dementia
Distribution of abnormalities -> clinical manifestations Dementias caused by abnormal accumulation of particular proteins/peptides Distribution of pathophysiological abnormalities generally correlates with distribution of histopathological abnormalities Same pathophysiological abnormalities can -> different clinical manifestations Different pathophysiological abnormalities -> same clinical manifestations Different types of dementia often co-exist
36
Distribution of abnormalities in dementia
Temporoparietal -> memory impairment, dysphasia, dyspraxia Frontotemporal -> behavioural disturbances, personality change, language dysfunction Subcortical -> slowing of thought processes, motor disturbances
37
Abnormal accumulation of particular proteins/peptides in dementia
Alzheimer's - Aβ plaques and hyperphosphorylated tau Frontotemporal dementia - FTLD-Tau - 3R, 4R or 3R + 4R Parkinson's disease, Lewy body dementia - Lewy bodies, diffuse plaques (exception is vascular dementia - no accumulation of peptides, mainly in white matter, microinfarcts) - atheroma and small vessel disease cause
38
Reticular formation
Set of interconnected nuclei located throughout brainstem Includes grey matter immediately below 4th ventricle and around cerebral aqueduct (= periaqueductal grey), and monoamine cell groups + non specific nuclei of thalamus, sometimes also hypothalamus considered Extends caudally into spinal cord
39
Local projections in reticular formation
Local-circuit interneurones Functions - reflexive and stereotyped behaviours involving face and head: > chewing, swallowing, vomiting > respiratory activities - cough, sneeze, hiccups > cardiovascular responses
40
Reticular formation ascending information to cortex
(reticular activating system) Functions: - sleep-wake cycle - mediates various levels of alertness and consciousness - wakefulness (in mid-line group of thalamus) - filters incoming stimuli to discriminate irrelevant background stimuli
41
Reticular formation descending information from spinal cord
Info from: - posture, equilibrium, autonomic nervous system activity - sensory (pain) and motor modulation Also receives information from hypothalamus
42
Overall functions of reticular formation
SENSORY AND MOTOR FUNCTIONS - gating + modulating info transfer - organising, co-ordinating reflexes AUTONOMIC AND VITAL FUNCTIONS - regulates autonomic nervous system - cardiovascular regulation - control of respiration ENERGISING/REGULATING FUNCTIONS - attention - alertness and sleep - motivation - general excitability in CNS (not specific targets, connections to whole cortex)
43
Neurotransmitter pathways and functions in reticular formation
NORADRENALINE From lateral tegmental system - to basal ganglia - autonomic, endocrine, appetite functions From locus ceruleus system - links all over cortex and cerebellum, so can synchronise brain regions - alertness, attention 5-HT, SEROTONIN From Raphe nucleus - to cerebellum and all over cerebral cortex - sleep, mood/motivation, autonomic NS, pain transmission ADRENALINE To hypothalamus - cardiovascular function DOPAMINE From substantia nigra to basal ganglia, and from ventral tegmental area to limbic areas and cortex - drive/motivation, pleasure (affected in schizophrenia, addiction) ACETYLCHOLINE From basal forebrain nucleus and septal nuclei to all cortex, and from septal nuclei to hippocampus - alertness/sleep, memory and learning
44
Cardiovascular control in reticular formation
(in medullary and lower pontine RF) INPUTS - baro-/chemoreceptors of aortic arch (via vagus) and carotid sinus (via glossopharyngeal) - autonomic activity from spinal cord - autonomic reflex afferents from vagus - blood and CSF composition from area postrema OUTPUTS - dorsal motor nucleus of vagus - sympathetic outflow in intermediolateral column in cord
45
Ventilatory control in reticular formation
MEDULLA - ventral respiratory group - voluntary forced exhalation, and to increase force inspiration - dorsal respiratory group - most inspiratory movements and timing PONS - pneumotaxic centre - coordinates inhale-exhale transition, inhibits inhalation, fine tunes respiration rate - apneustic centre - coordinates inhale-exhale transition, stimulates inhalation (overridden by pneumotaxic control to end inspiration)
46
Brainstem lesions and effects on respiratory system
i) Diffuse forebrain depression -> waxing/waning respiration pattern, periods of apnea, Cheyne-Stokes respiration ii) Midbrain damage -> hyperventilation iii) Rostral pons damage -> apneusis, briefly halts breathing at full inspiration iv) Lower pons or upper medulla damage -> irregular/uneven depth respiration, ataxic breathing Often -> respiratory arrest
47
Glasgow coma scale
= GCS, coma is score less than 8 ``` Eye opening (E) 4 = spontaneous 3 = to voice 2 = to pain 1 = absent ``` ``` Vocal response (V) 5 = normal conversation 4 = disoriented 3 = incoherent words 2 = incomprehensible sounds 1 = absent ``` ``` Motor response (M) 6 = normal 5 = localised response to pain 4 = withdrawal from pain 3 = rigidity with limb flexion 2 = rigidity with limb extension 1 = absent ```
48
Sleep
Light - easily awakened Deep - needs strong sensory stimulus for arousal REM - 5-30min periods every 90 mins, deep sleep, cerebral cortex very active, dreaming, muscular relaxation - > decreased plasma volume - > decreased HR - > decreased bp - > decreased rate and force of respiration - > decreased salivary and lacrimal secretion - > decreased formation of urine - > increased sweat secretion - > decreased muscle tone and reflexes (except ocular muscles)
49
EEG
= electroencephalogram - shows changes in level of consciousness, activity in cerebral cortex ``` Fully alert - low voltage, high frequency Deep sleep - taller, longer waves REM sleep - desynchronised Comatose - reduced voltage and frequency Cerebral cortex death - flat EEG ```
50
Types of sleep disorder
Insomnia - difficulty falling/staying asleep Hypersomnia - excessively sleepy Narcolepsy/cataplexy - excessively sleepy, daytime sleep attacks Sleep apnea - pauses or low frequency breathing during sleep Night terror - extreme terror, temporary inability to regain full consciousness Somnambulism - sleep walking Nocturnal enuresis - bed wetting Movement disorders

2nd Year - Systems 3 (10 decks)

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