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CSB601 > Week 11: Neurology - Epilepsy, Parkinson's Disease, Dementia > Flashcards

Week 11: Neurology - Epilepsy, Parkinson's Disease, Dementia Flashcards

1
Q

What is dementia?

A

Dementia is a clinical syndrome that is characterized by progressive deterioration in cognition with resulting decline in function

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2
Q

Cognitive Impairment symptoms of dementia

A
  • Cognitive impairment is the hallmark of dementia
  • Trouble remembering new info
  • Problems with speech and language
  • Spacial disorientation
  • Significant problems with long term memory
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3
Q

Neuropsychiatric symptoms of dementia

A
  • Mood changes
  • Delusions
  • Hallucinations
  • Shouting and agitation
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4
Q

What are the causes of dementia

A

5 major causes

  • Most common is Alzheimer’s disease
  • Vascular dementia
  • Primary frontal dementia
  • Dementia with Lewy bodies and Parkinson’s disease dementia
  • Alcohol related dementia
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5
Q

Pathophysiology of Alzheimer’s

A
  • Abnormal build up of proteins (increase amyloid plaques and Tau tangles) causing neuronal death
  • Brain atrophy causing loss of inter-neuronal communication
  • Neurochemical changes (decreased acetylcholine signalling) causing loss of inter-neuronal communication
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6
Q

Dementia - Non pharmacological interventions

  • Aims
  • Options
A

Not one size fits all - address patient overall well being rather than specific symptoms

Aims:

  • Reduce distress
  • Improve function
  • Improve cognition
  • Care giver support
  • Improve quality of life

Options

  • Memory training
  • CBT
  • Environmental modification
  • Alternative therapies
  • Behavioral management therapy
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7
Q

Dementia Pharmacological Management

- Neuropsychiatric symptom options

A
  • Pharmacological interventions best reserved for exceptional circumstances
  • Atypical antipsychotics (Risperidone) can manage hallucinations, delusions and disturbed behavior
    > Associated with increase risk of mortality
  • Benzodiazepines (Oxazepam) can manage anxiety and agitation
    > Exacerbate cognitive impairment and increase fall related injuries
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8
Q 
Dementia Pharmacological Management
- Cognitive impairment aims
- Options
> Example
> MOA
> ADR
> Practice point
A

Aims

  • Offer a modest improvement in cognition and function
  • Does not modify underlying progression of dementia
  • Specifically benefits patients with dementia caused by Alzheimer’s

Options
- Acetylcholinesterase inhibitors
> Donepezil, Galantamine, Rivastigmine
> MOA = increase synaptic concentration of acetylcholine by reducing its enzymatic breakdown through inhibition of acetylcholinesterase
> ADR = Gastrointestinal
> Practice point = Good adherence is important due to tolerability
- NMDA antagonist
> Memantine
> MOA = Antagonise NMDA receptor reducing glutamate-induced neuronal degradation

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9
Q

How does the brain communicate?

A

Between neurons is chemical impulse
Through neurons is electrical impulse

Process

  • Electrical impulse
  • Vesicular fusing
  • Neurotransmitter binding
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10
Q

Electrical impulse in brain

A
  • Excitation neurotransmitter bind to post synpatic neuron causing influx of positive charged ions
  • Nearby voltage gated sodium channels open allowing more positively charged sodium to enter neuron
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11
Q

Vesicular fusing in brain

A
  • Electrical impulse reaches end of neuron, there is a resultant opening of voltage gated calcium channels
  • Influx of calcium causes vesicle to fuse with pre synaptic membrane
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12
Q

Neurotransmitter binding in brain

A
  • Excitatory neurotransmitters bind to post synaptic neuron and cause influx of positively charged ions
  • Inhibitory neurotransmitters bind to post synaptic neuron and cause influx of negatively charges ions
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13
Q

What is epilepsy?
(Characterized by)
What is a seizure?

A
  • Disease of brain characterized by either the following
    > At least two unprovoked seizures occurring >24 hrs apart
    > One unprovoked seizure and risk of further seizures
    > Diagnosis of epilepsy syndrome

Seizures are transient occurrence of signs and/or symptoms due to abnormally excessive or synchronous neuronal activity in brain
- Seizure threshold is lowered by pharmacological substances, sleep deprivation, fasting/malnutrition, psycho physiological stress, fever, menstruation

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14
Q

Classification of seizure types

A

Focal onset

  • Aware/Impaired awareness
  • Motor onset/Non motor onset
  • Focal to bilateral tonic-clonic

Generalized onset
- Motor/Non motor

Unknown onset

  • Motor/Non motor
  • Unclassified
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15
Q

Epilepsy is an umbrella term

- What are the classifications of epilepsy’s?

A
  • Seizure type
  • Epilepsy type
  • Epilepsy syndrome
  • Aeitology
  • Comorbidities
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16
Q

Epilepsy - Pharmacological intervention

  • Goal of therapy
  • Common drug classes used
A

Goals are to

  • Suppress seizures
  • Avoid adverse effects

Drug classes

  • Barbituates
  • Benzodiazepines
  • Other antiepileptics
17
Q

Epilepsy - Voltage gated sodium channel blockers

  • Example
  • MOA
  • Adverse effect
  • Practice points
A

Example
- Carbamazepine

MOA
- Prevent excessive neuronal communication through inhibition of voltage gated sodium channels

Adverse effects
- Many and some very serious

Practice points

  • Lots of monitoring
  • Strong CYP inducer - many interactions
  • Can also be used to manage pain and bipolar disorder
18
Q

Epilepsy - Voltage gated calcium channel blockers

  • Example
  • MOA
  • Adverse effect
  • Practice points
A

Example
- Gabapentin

MOA
- Prevent excessive neuronal communication through inhibition of voltage gated calcium channels

Adverse effects
- Many

Practice point
- Can also be used to manage neuropathic pain

19
Q

Epilepsy - GABA enhancers

  • Example
  • MOA
  • Adverse effect
  • Practice points
A

Example
- Benzodiazepines (Clonazepam, Midazolam)

MOA
- Prevent excessive neuronal communication by enhancing effects of inhibitory neurotransmitter GABA

Adverse effects
- Highly sedating

Practice points

  • Also used in wide range of psychiatric indications
  • Is dependence a concern?
20
Q

Epilepsy - Broad spectrum anti-epileptic

  • Example
  • MOA
  • Adverse effect
  • Practice points
A

Example
- Sodium valproate

MOA
- Prevent excessive neuronal communication by inhibiting voltage gated sodium channel, inhibiting voltage gated calcium channels and enhancing effects of GABA

Adverse effects
- Many and some very serious

Practice point

  • Lots of monitoring
  • Can be used in migraines and bipolar disorder
21
Q

Physiology of dopamine

  • Dopamine degradation process
  • Dopamine receptors
A

Dopamine is a catecholamine neurotransmitter involved in movement, mood, prolactin release and emesis

It is degraded by both MAO and COMT

  • MAO-A - expressed in CNS and periphery
  • MAO-B - concentrated in CNS only and responsible for degradation of most CNS dopamine

There are 5 dopamine receptors (focus on two)

  • D1 is positively coupled to adenylate cyclase which activates signalling and is excitatory
  • D2 is negatively coupled to adenylate cyclase which inhibits signalling
22
Q

Direct dopamine pathway

Indirect dopamine pathway

Nigrostriatal Pathway

A

Direct pathway

  • Utilizes D1 receptor
  • Stimulated by dopamine release
  • Enables normal movement

Indirect pathway

  • Utilizes inhibitory D2 receptor
  • Inhibited by dopamine
  • Inhibits movement (removes pathways inhibition of movement and therefore allows normal movement)

Both use the nigrostriatial pathways (extrapyramidal system) to control movement - purposeful movement and keeping muscles stable at rest
- Balance between the two allows smooth coordinated movement

23
Q

Pathophysiology of Parkinson’s disease

A

Slow, progressive neurodegenerative disease of extra pyramidal motor system

Selective loss of dopaminergic neurons in CNS, especially in nigrostriatal pathway which controls movement
- Loss of dopamine in substantia nigra
> Can no longer activate excitatory D1 pathway reducing ability for normal movement
> Can no longer inhibit inhibitory D2 pathway which allows this pathway to take over/stay on thus further reducing movement

24
Q

PD symptoms

  • Non motor
  • Motor
A

Non motor

  • Sleep disturbance (insomnia, restless leg syndrome)
  • Nausea, fatigue, speech problems, pain, dysesthesias
  • Autonomic symptoms (drooling, constipation, sexual dysfunction, urinary problem, sweating, orthostatic hypotension, dysphagia)
  • Psychological symptoms (anxiety, psychosis, cognitive impairment, depression)

Motor’

  • Tremor at rest
  • Rigidity
  • Akinesia
  • Bradykinesia
  • Difficulty standing up straight
  • Gait abnormalities
25
Q

Pharmacotherapy of PD

- Individualization

A

Initial choice is about individualization (age, occupation and activity, economic situation, presence of cognitive decline, level of functioning)

  • All therapies lose effectiveness over time
  • Delay treatment until symptoms distressing or impact daily functioning

Start low go slow
Benefits may take weeks to see effect

26
Q

Pharmacotherapy of PD

- Options

A
  • Levodopa
  • COMT inhibitor
  • Dopamine agonist
  • Anticholinergic drugs
  • Selective MAO-B inhibitors

Surgical options

  • Deep brain stimulation
  • Ablative lesioning
27
Q 
Pharmacotherapy of PD;
Dopamine precursors
- MOA
- Example
- Practice points
- Adverse effects
A

MOA
- Gets converted to dopamine both in periphery and CNS (active transporters for levodopa across BBB but dopamine cannot cross)

Example
- Levodopa

Practice point

  • First line in most patients
  • Co administered with dopa decarboxylase inhibitor to prevent peripheral breakdown

Adverse effects

  • Many
  • Nausea
  • Hallucinations
  • Insomnia
  • Dyskinesia (worsens as disease progresses and is common)
  • As levodopa effect wears off (reaches max effect) it causes on/off symptoms - patient looses ability of normal movement
28
Q 
Pharmacotherapy of PD;
COMT inhibitors
- MOA
- Example
- Practice points
A

MOA
- Inhibit COMT from being able to break down dopamine in CS and levodopa in periphery

Example

  • Entacapone
  • Tolcapone

Practice points
- Not used as single therapy, always given with levodopa

29
Q 
Pharmacotherapy of PD;
Dopamine agonists
- MOA
- Example
- Practice points
A

MOA
- Stimulate dopamine receptors to make more responsive to dopamine signalling

Examples

  • Pramiprexole
  • Bromocriptine
  • Cabergoline

Practice point
- Lots of psychiatric ADR

30
Q 
Pharmacotherapy of PD;
Anticholinergics
- MOA
- Example
- Practice points
A

MOA
- Help rebalance signalling of cholinergic dopaminergic neurons in PD

Example

  • Benzatropine
  • Benzhexol

Practice points

  • Make cognitive impairment worse
  • Never to be used with patients that have dementia/Alzheimer’s
  • Not to be used in patients with heart disease
31
Q 
Pharmacotherapy of PD;
MAO-B inhibitors
- MOA
- Example
- Practice points
A

MOA
- Inhibit MAO-B therefore reduce breakdown of dopamine in CNS and may block DA reuptake

Example

  • Selegiline
  • Rasagiline

Practice points
- Selective for MAO-B they have fewer ADR than non selective MAOIs used in depression

CSB601 (12 decks)

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