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Neurological, neuromuscular and musculoskeletal disease > PBL 45 > Flashcards

PBL 45 Flashcards

1
Q

What are the 5 most common subtypes of dementia?

A
  1. Alzheimer’s disease
  2. Vascular dementia
  3. Dementia with Lewy bodies
  4. Frontotemporal dementia
  5. Mixed dementia
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2
Q

Dementia vs mild cognitive impairment?

A

MCI = symptoms worse than affected for their age BUT ADLs are not affected

Dementia = The symptoms must have become bad enough to significantly affect the person’s ADL

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3
Q

Symptoms of dementia

A
  1. Memory problems
    - Retention of new information
    - Forget names
    - Lost in prev. familiar places
  2. Impairments in cognitive abilities
    - Disorientation in time and place
    - Concentration
    - Reasoning and decision-making skills
  3. Impairments in communication
    - Repetitive
    - Reading and writing
    - Following and engaging in conversation
  4. Changes in behaviour/personality
  5. Mood swings
  6. Anxiety/depression
  7. Lose interest in seeing others socially –> Isolation/withdrawal
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4
Q

Pathophysiology of Alzheimer’s disease

A

Physical changes in the structure of the brain:

  1. Amyloid plaques
    - Amyloid protein protects neurons from calcium influx and over-excitation by glutamate
    - Abnormal amyloid protein allows calcium influx and neuronal cell death
    - Abnormal amyloid protein processing allows a build up of BETA-amyloid which is laid down in neurons and deposited as plaques, these plaques lead to further inflammatory response which leads to further cell death and disruption to function
  2. Tau - neurofibrillary tangles
    - Tau protein helps brain cells communicate with each other
    - Hyperphosphorylated tau leads to a build-up of tau protein which causes tangles, this makes the cells less able to communicate with each other
  3. Reduced acetylcholine
    - Leads to information less likely to be transmitted, or not at all
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5
Q

Which of the general symptoms of dementia are more common in Alzheimer’s?

A

Memory lapses due to hippocampal changes (STM), these also lead to disorientation in time and place, or not being able to recognise familiar faces and objects

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6
Q

Risk factors for Alzheimer’s disease

A
  1. Age - >65y/o
  2. Sex - Women > men
  3. Genetics - RARE
  4. Poor physical health - Inadequately controlled heart disease or diabetes
  5. Lifestyle choices - smoking, lack of exercise, Xs alcohol use
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7
Q

What has to be ruled out when diagnosing Alzheimer’s?

A
  • Vitamin B-12 deficiency

- Underactive thyroid gland

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8
Q

Prevention of Alzheimer’s?

A
  1. Regular health checks with GP
  2. Keep on top of physical health conditions
  3. Mediterranean diet
  4. Have BP, weight and cholesterol regularly checked
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9
Q

First line treatment for Alzheimer’s? MoA, side effects and contraindications

A

ACETYLCHOLINESTERASE INHIBITORS
- Donepezil / Rivastigmine / galantamine

MoA: Reduce breakdown of Ach in synaptic cleft to support cell communication

Side effects: GI = Nausea, vomiting, diarrhoea

Contraindications: Asthma/COPD, seizures, arrhythmias

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10
Q

Alternative treatment for Alzheimer’s disease (behavioural symptoms). Side effects and contraindications?

A

MEMANTINE
Side effects: sleepiness, sedation, dizziness, headache, constipation, SOB

Contraindications: Seizures

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11
Q

MoA of memantine

A

NMDA (glutamate) receptor antagonist

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12
Q

What is vascular dementia?

A

An umbrella term for a group of conditions caused by problems with blood circulation to the brain

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13
Q

Pathophysiology of vascular dementia

A
  • TIAs - prevent O2 reaching brain tissue
  • Atherosclerosis - blocked arteries
  • Haemorrhage
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14
Q

Signs and symptoms of vascular dementia (different to Alzheimer’s)

A
  • Confusion
  • Agitation
  • Depression
  • Unsteady gait
  • Memory problems
  • Urinary frequency, urgency and incontinence
  • Night wandering
  • Decline in ability to organise thoughts/actions, difficulty organising
  • Poor attention & concentration
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15
Q

Risk factors for vascular dementia

A
  1. Age - >65y/o
  2. Sex - Men>women
  3. FHx - Stroke, diabetes, CV disease
  4. Poor physical health - Inadequately controlled CV disease, diabetes, hypertension, hypercholesterolaemia
  5. Lifestyle choices - Smoking, Xs alcohol use, lack of exercise
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16
Q

Treatment for vascular dementia

A

INFARCT DAMAGE CANNOT BE REVERSED

  • Manage/control the risk factors!
  • Manage physical conditions (diabetes, blood pressure, hypercholesterolaemia, weight)
  • Mediterranean diet
  • Lifestyle changes - stop smoking, less alcohol use, weight reduction/exercise
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17
Q

Pathophysiology of dementia with Lewy bodies (DLB)

A

Build-up of clumps of proteins called Lewy bodies in nerve cells, this disrupts how cells communicate with each other

Lewy bodies are also linked to a decrease in certain chemicals, particularly acetylcholine and dopamine, causing a loss of connection between nerve cells

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18
Q

What are Lewy bodies?

A

A build-up of alpha synuclein protein which are deposited in nerve cells

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19
Q

Signs and symptoms of DLB

A

Depends where the Lewy bodies have accumulated within the brain

  • Those found at the base of the brain have been linked to PARKINSONIAN features = slowed movement, stiffness, tremors
  • Increased falls
  • Well-formed hallucinations
  • Delusions
  • Early visuospatial awareness problems
  • General dementia symptoms: mood changes, memory problems, fluctuating alertness / confusion / concentration levels, problem solving skills decline
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20
Q

Risk factors for DLB

A
  1. Age - >65y/o
  2. Sex - EQUALLY men and women
  3. Genetics - RARE
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21
Q

A diagnosis of DLB requires a progressive decline in your ability to think and at least two of what?

A
  1. Fluctuating alertness and thinking function
  2. Repeated visual hallucinations
  3. Parkinsonian features
  4. REM sleep behaviour disorder - where people act out their dreams during sleep
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22
Q

Treatment/management for DLB

A

There is NO SPECIFIC treatment

  • Hearing and sight problems make delusions and hallucinations worse, so tend to these!
  • Sleep problems can be an issue, so reduce caffeine & alcohol intake later in the afternoon, keep bedroom at a comfortable temperature and reduce unnecessary stimuli
  • Can use acetylcholinesterase inhibitors for memory/attention/hallucination problems
  • PARKINSON’S DISEASE MEDICATION - L-dopa for the Parkinsonian symptoms however this can increase confusion, hallucinations and delusions
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23
Q

What are the 3 variants of frontotemporal dementia?

A
  1. Behavioural variant frontotemporal aphasia (Pick’s disease)
  2. Primary progressive aphasia = semantic dementia and progressive non-fluent aphasia
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24
Q

Pathophysiology of frontotemporal dementia

A

Occurs when nerve cells in the frontal or temporal brain lobes die
- This causes chemical messengers which transmit signals between these two lobes to be lost, so over time there is more and more cell death, causing the volume of the brain tissue in the frontal and temporal lobe to shrink!

  • ASSOCIATED WITH MUTATION IN TAU GENE
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25
Q

Signs and symptoms of frontotemporal dementia (behavioural variant)

A
  • Changes in personality and behaviour –> lose inhibitions
  • Apathy and withdrawal
  • Obsessive or repetitive behaviour
  • Loss of empathy, emotional blunting
  • Changes in appetite and food eaten –> hyperorality
  • Difficulties with decision making, problem solving and concentration
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26
Q

Signs and symptoms of frontotemporal dementia (primary progressive aphasia)

A
  • Language difficulties
  • Speech
  • Grammar problems
  • Reduced comprehension
  • Loss of understanding of familiar words
  • Difficulty recognising people or objects
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27
Q

Risk factors for frontotemporal dementia

A
  • Sports where you are constantly being hit in the head
  • Age - <65y/o
  • Sex - Men and women equally
  • Genetics - 1/3 cases may be familial
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28
Q

What are the principal classes of anaesthetic drugs?

A
  1. General anaesthesia
  2. Local anaesthetic agents
  3. Neuromuscular blocking drugs
  4. Analgesia
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29
Q

Anaesthesia is a triad of…

A
  1. Hypnosis
  2. Areflexia
  3. Analgesia
30
Q

What is the main characteristic of general anaesthetics that allow them to be effective?

A

They are HIGHLY lipid soluble

31
Q

Which receptors do general anaesthetic agents work on?

A

GABA

32
Q

Give some examples of desirable effects of general anaesthetics

A
  1. Unconsciousness
    - Reticular formation
    - Thalamic sensory relay nucleus
    - Cortex
  2. Loss of reflexes
  3. Analgesia
33
Q

Give some side effects / UNdesirable effects of general anaesthetic agents

A
  • Decreased cardiac contractility
  • Sympathetic inhibition
  • Respiratory depression
  • In higher concentrations, all brain functions are depressed –> death
34
Q

Examples of volatile and IV general anaesthetic agents

A

Volatile: nitrous oxide

IV: propofol, ketamine, thiopentone

35
Q

MoA of local anaesthetic agents

A

Block voltage gated Na+ channels causing a patch of numbness

36
Q

What are the two classes of neuromuscular blocking drugs?

A

Depolarising

Non-depolarising

37
Q

Example of local anaesthetic agent

A

Lidocaine

38
Q

MoA of depolarising neuromuscular blocking drugs (Use example)

A

Suxamethonium

  • It is 2 Ach molecules bound together
  • Activates nAchR causing depolarisation
  • DOES NOT UNBIND
  • You get fasciculations, bradycardia (acts on mAchR) and K+ efflux
39
Q

MoA of non-depolarising neuromuscular blocking drugs (Use example)

A
  • Quaternary ammonium compounds = turbocurarine, rocuronium, atracurium, vecuronium
  • Competitively bind to the nAchR in the post-synaptic junction
  • DO NOT cause activation of the receptor, hence they are called non-depolarising
  • Do not get the fasciculations, K+ efflux and bradycardia as with depolarising drugs
40
Q

Can acetylcholinesterase inhibitors be used as neuromuscular blocking agents?

A

YES, increasing Ach levels in the synaptic cleft allow activation of nAchR and depolarisation followed by paralysis
- Such as pyridostigmine and neostigmine

41
Q

What is a seizure?

A

Abnormal paroxysmal discharge/electrical activity of cerebral neurons sufficient to cause clinically detectable intermittent disturbance of consciousness, behaviour, emotion, motor or sensory function

42
Q

What is epilepsy?

A

A condition in which seizures recur, usually spontaneously

43
Q

Pathophysiology of epilepsy

A
  • Pyramidal cells are the main excitatory cells
  • Basket cells inhibit/regulate cortical activity
  • De-regulation of basket cells leads to uncontrolled pyramidal activity
  • So you get inward currents and >glutamate coupled with a lack of GABA activity
44
Q

Epilepsy can be classified according to impairment type and EEG localisations, what are the main classifications?

A
  1. Generalised

2. Partial/focal

45
Q

What is the most common type of epilepsy?

A

Generalised

46
Q

What is meant by generalised epilepsy? Explain the 4 subtypes

A

This is when the electrical discharge starts in the centre of the brain and spreads to all parts of the cortex

  1. Tonic clonic
    - Alternate contraction and extension of muscles (tonic = stiff, clonic = jerk)
    - Loss of consciousness
  2. Absence
    - Individuals appear ‘absent’ for a while
  3. Myoclonic
    - Causes muscle spasms
  4. Atonic
    - Involves loss of muscle activity for >1 second, individual may collapse
47
Q

What is meant by partial epilepsy? What are the three subtypes?

A

Partial/focal epilepsy is when the electrical discharge arises in a single lobe in the brain

  1. Simple partial
    - No loss of consciousness or awareness
    - A general strange feeling & rising feeling in stomach
    - Deja vu
    - Unusual smell or taste
    - Tingling
    - Intense feeling of fear or joy
    - Stiffness
  2. Complex partial
    - Affects single lobe but individual loses awareness - becomes dazed, gets an aura (odd taste/smell) before becoming dazed but does not lose consciousness
    - Smacking lips
    - Rubbing hands
    - Making random noises
    - Moving your arms around
    - Picking at clothes
    - Chewing or swallowing
    - You will not be able to reply to people and you will have no memory of the seizure afterwards
  3. Partial with secondary generalisation
    - Seizure arises in 1 lobe but spreads to all of the brain
48
Q

Causes of epilepsy? Aetiology/pathology

A
  1. Hippocampal sclerosis
  2. Malformations of cortical development
  3. Tumours
  4. Vascular malformations
  5. Cerebrovascular disease
  6. Post-traumatic
  7. Inflammatory - post-infective or autoimmune
49
Q

Triggers for an epileptic seizure?

A
  • Lack of sleep
  • Psychological and emotional stress
  • Other medications
  • Metabolic derangements
  • Hormonal changes
  • Alcohol and recreational drugs
  • Stimulants
50
Q

Characteristics of a frontal lobe seizure

A
  1. Hyperkinetic activity
  2. Expressed fear
  3. Speech arrest
51
Q

Characteristics of a parietal lobe seizure?

A
  1. Sensory disturbance - paraesthesia
  2. Rigorous and consistent sensory disturbance in one of the other limbs
  3. Motor activity affected following 50% of cases
52
Q

Characteristics of a temporal lobe seizure

A
  • CONNECTED TO THE AMYGDALA, SO HAS LIMBIC FEATURES
  • Emotional disturbance
  • Deja vu
  • Metal taste in mouth
  • 1-2mins
  • Speech arrest
  • Motionless stare
  • Automatism
  • Post ictal confusion, headache, dysphasia and nose rubbing
53
Q

What is automatism?

A

Feature of temporal lobe seizures

  • Lip smacking
  • Fidgeting
  • Fumbling
  • Chewing or swallowing
54
Q

A partial seizure WITH automatism is a feature of epilepsy affecting which lobe?

A

Temporal lobe

55
Q

A partial seizure WITHOUT automatism is a feature of epilepsy affecting which lobe?

A

Frontal

56
Q

Management of epilepsy

A 
Lamotrigine
Levetiracetam
Sodium valproate
Benzodiazepine
Gabapentin
Carbamazepine
Oxycarbazepine
Topiramate
57
Q

MoA of lamotrigine

A

Na+ channel blocker

- Inhibits sodium currents which causes the suppression of glutamate

58
Q

MoA of levetiracetam

A

Binds to SV2A, modulating synaptic neurotransmitter release

- Increases the amount of GABA to tone down nerve signalling and reduce seizure activity

59
Q

MoA of sodium valproate

A

Converted into its active form valproate ion

  • Increases GABA concentration in the brain
  • Inhibits the enzymes responsible for catabolism of GABA
  • Increases outward positive current (K+)
60
Q

What are the targets for anti-epileptic drugs?

A
  1. Increase GABA (inhibitory neurotransmitter)
  2. Decrease glutamate (excitatory neurotransmitter)
  3. Block voltage-gated inward positive currents (Na+ or Ca2+)
  4. Increase outward positive current (K+)
61
Q

Give examples of anti-epileptic drugs which increase GABA concentrations. Give an explanation of how they do so.

A
  1. Benzodiazepines
    - Increase GABA-mediated chloride channel openings
  2. Valproate
    - Increase levels of GABA and block VG Na+ channels
  3. Gabapentin
    - GABA analogue
62
Q

Give examples of anti-epileptic drugs which decrease glutamate activity. Explain how each one does so.

A
  1. Carbamazepine
    - Blocks VG Na+ channels
  2. Oxcarbazepine
    - Blocks VG Na+ channels
63
Q

What are pleiotropic AEDs? Give an example

A

AEDs affecting multiple systems
- TOPIRAMATE
Blocks Na cahnnels and increases the frequency at which GABA opens chloride channels

  • Valproate
    Enhances GABA transmission, blocks Na+ channels
64
Q

Symptoms of TACS (total anterior circulation stroke)

A

All 3 of:

  1. Unilateral weakness (and/or) sensory deficit of face/arm/leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction (e.g dysphasia)
65
Q

Symptoms of PACS (partial anterior circulation stroke)

A

2 of the following:

  1. Homonymous hemianopia
  2. Unilateral weakness (and/or) sensory deficit of face/arm/leg
  3. Higher cognitive dysfunction (e.g dysphasia)
66
Q

Symptoms of POCS (posterior circulation stroke)

A

1 of the following:

  1. Cranial nerve palsy with contralateral motor/sensory deficit
  2. Bilateral motor/sensory deficit
  3. Conjugate eye movement disorder
  4. Cerebellar dysfunction (VANISH’D)
  5. Isolated homonymous hemianopia
67
Q

Symptoms of LACS (lacunar syndrome)

A

1 of the following:

  1. Pure sensory stroke
  2. Pure motor stroke
  3. Sensory-motor stroke
  4. Ataxic hemiparesis
68
Q

Which part of the brain circulation is affected by TACS?

A

ACA or MCA

69
Q

Which part of the brain circulation is affected by PACS?

A

ACA

MCA

70
Q

Which part of the brain circulation is affected by LACS?

A

Deep perforating arteries

71
Q

Which part of the brain circulation is affected by POCS?

A

Vertebrobasilar arteries

Neurological, neuromuscular and musculoskeletal disease (36 decks)

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