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MPharm Y3S2 > Clinical CNS Parkinson's > Flashcards

Clinical CNS Parkinson's Flashcards

1
Q

Define PD:

A

A chronic progressive neurodegenerative condition resulting from the loss of the dopamine containing cells of the substantia- nigra
The resulting dopamine deficiency within the basal ganglia leads to movement disorders

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2
Q

Describe the prevalence of PD:

A

2nd most common neurodegenerative disease after AD
Around 137,000 pts with PD in UK
Lifetime risk of being diagnosed with PD is 2.7% (1in 37 people)
Increasing prevalence with age (over 80)
More common in men than women

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3
Q

What is early onset PD?

A

1 in 20 patients diagnosed before 40 years old

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4
Q

What are the different classes of clinical presentation in PD?

A

Motor symptoms
Non-motor symptoms

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5
Q

Name the motor symptoms of PD:

A

Bradykinesia
Muscle rigidity
Tremor

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6
Q

What is Parkinsonism?

A

All of the motor symptoms
PD is a type of Parkinsonism but there are other causes e.g drug induced Parkinsonism, stroke

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7
Q

Name the non-motor symptoms of PD:

A

Depression/anxiety
Fatigue
Cognitive impairment/ dementia
Sleep disturbance
Constipation
Dysphagia
Weight loss
Hyposmia (decrease sense of smell)
Sialorrhoea (drooling/ excessive salivation)
Excessive sweating
Urinary/bladder problems
Pain
Hypotension

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8
Q

Name and describe the different dopaminergic pathways leading to PD symptoms:

A

Motor control (nigrostriatial system)
Behavioural effects (mesolimbic and mesocortical pathways)
Endocrine control (tuberohypophyseal system)

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9
Q

Define bradykinesia:

A

Slowness of voluntary movement
This can be asymmetrical and unpredictable

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10
Q

Describe the symptoms of bradykinesia:

A

Mask like face/ limited expressions/ limited blinking
Hypophonia (soft voice) and/ or monotonous voice
Micrographia (small handwriting)
Difficulty performing fine motor actions (e.g fastening buttons/ shoelaces)
Walk with a shuffling gait (take smaller steps than normal)

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11
Q

Describe what rigidity is:

A

Increase in muscle tension
Characteristic of stooping posture
Rigidity affects balance, increased risk of falls (harmful as slow reactions due to bradykinesia)
Associated with muscle pain

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12
Q

What areas does rigidity commonly affect in PD?

A

Mostly affects flexor muscles of trunk and limbs
Flexor= any muscle that decreases the angle between bones on 2 sides of a joint e.g elbow/ knee

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13
Q

Describe the symptoms of a tremor in PD:

A

Not all PD patients will have a tremor
Resting tremor, normally in one or both hands, stops with voluntary movement or mental concentration
‘Pill rolling’, fingers roll in a circular movement as in rolling fingers between thumb

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14
Q

What areas does a tremor commonly affect in PD?

A

Hands
May affect:
-chin, lips, face and legs
May appear unilaterally

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15
Q

Name common drugs that can cause a SE of tremor:

A

Antipsychotics normally in first 10 weeks of taking and more common in 1st gen e.g haloperidol, chlorpromazine- generally dose related and reversible
B agonists e.g salbutamol/ salmeterol
Antiemetics e.g prochlorperazine, metoclopramide
Co-trimoxazole, SSRIs, lithium, valporic acid, medroxyprogesterone

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16
Q

What are the extrinsic aetiology’s of PD?

A

Most causes idiopathic
Environmental and physical

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17
Q

What is the environmental aetiology of PD?

A

Prescription drugs- all of above+ reserpine and tetrabenazine
Recreational drugs

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18
Q

What is the physical aetiology PD?

A

Cerebral ischaemia
Viral encephalitis
Brain stem injury
Dementia pugilistica

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19
Q

What are the intrinsic aetiology’s of PD?

A

Genetic- 10% inherited/ DNA damage
Age

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20
Q

What is the genetic aetiology of PD?

A

a-synuclein point mutations
Lewy body formation
Parkin gene mutation (early onset)

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21
Q

Describe the Parkin mutation in PD:

A

Mutation in parkin, most common cause of early onset disease
Enzymatic protein, maintaining mitochondrial quality control
Encoded by PARK2 gene
Neuroprotective protein- against a-synuclein

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22
Q

How can reserpine and tetrabenazine cause Parkinsonism like symptoms?

A

Depletes monoamines from pre-synaptic storage, decreases dopamine release

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23
Q

How can recreational drugs cause Parkinsonism like symptoms?

A

MPTP (contaminant found in MPPP ‘synthetic heroin’)- metabolite kills dopamingeric neurons in the substantia nigra, sudden irreversible Parkinsonism

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24
Q

What physical symptoms can cause Parkinsonism?

A

Dementia Pagilistica- late onset syndrome of dementia and Parkinsonism
Occurrence associated with multiple concussions/ head injuries e.g professional fighters
Other head trauma affecting the aopaergic system- head injury/ stroke

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25
Q

Describe how viral illnesses can cause Parkinsonism:

A

Encephalitis lethargica epidemic- aka sleeping sickness
Killed 500,000 people worldwide
Symptoms were severe Parkinsonism
Increase drowsiness and rigidity
Sufferers gradually ‘seized up’
Eventually catatonic- state of permanent rigidity
Short term relief from L-dopa

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26
Q

Describe the diagnosis for PD:

A

Normally present in primary care
Refer urgently and untreated to a specialist (neurologist/ geriatrician)
No conclusive diagnostic test
Diagnosis will be decided on symptoms, medical history and a detailed neurological examination

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27
Q

Name and describe the neurological examinations that occur for a PD diagnosis:

A

Brain scans e.g MRI- exclude differential diagnosis
Dopamine Transporter scan (DaTSCAN)- measures density of nigrostriatial dopamine transporter sites:
-but abnormal DaTSCAN can’t solely confirm diagnosis as similar loss can occur in other neurological conditions
-not routinely performed a not recommended by NICE
An improvement in symptoms upon starting parkinsons med will support a diagnosis of PD

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28
Q

What are the steps in diagnosing PD?

A

Step 1: Diagnosis of parkinsonian syndrome- motor symptoms
Step 2: Exclusion criteria
Step 3: Supportive criteria

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29
Q

What is the first line treatment in PD with motor symptoms?

A

Offer Levodopa to patients with early PD whose motor symptoms affect their QoL
Consider a choice of dopamine agonists, L dopa, or MAO-B inhibitors with early PD whose motor symotms don’t affect QoL

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30
Q

What is the adjuvant therapy in PD with motor symptoms?

A

Offer a choice of dopamine agonists, MAO-Bi or COMTi as an adjunct to L dopa
If dyskinesia is not adequately managed by modifying existing therapy, consider amantadine

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31
Q

Describe the use of L-dopa in PD:

A

Dramatically improves motor function (around 80%), 20% restored to normal motor function
Palliative treatment- no effect on disease progression
Effectiveness decreases with time, must escalate dose:
-receptor down regulation
-disease progression

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32
Q

When should you start L-dopa?

A

Different for every patient
e.g older patient may want to start asap but younger may want to start it later

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33
Q

What are the unwanted SEs of L-dopa?

A

Dyskinesia (involuntary movements)
Fluctuations in clincal state
Acute SEs

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34
Q

Describe the dyskinesia SE for L-dopa:

A

From 2 years of starting (50% of patients by year 5)
Affects face, arm and trunk (limbs)

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35
Q

Describe the fluctuations in clinical state SE for L-dopa:

A

‘On-off’ phenomena (bradykinesia/ rigidity suddenly worsen then better)
Wearing off effect (end of dose deterioration)
Freezing

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36
Q

What are possible solutions for PD patients when they get symptoms due to wearing off their medication?

A

Mainly long term
Night and first thing in the morning as its the longest time without medication
Using SR or COMTi (entacapone) can help stop this

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37
Q

Describe the acute SEs for L-dopa:

A

Nausea and anorexia
Hypotension
Sleep disturbances including sudden onset of sleep implications for driving
Psychological effects- anxiety/ depression, schizophrenia symptoms

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38
Q

Name inhibitors that is given with L-dopa to inhibit the metabolism and why?

A

Dopadecarboxylase inhibitors:
-carbidopa
-benserazide
L-dopa is always given in combo with one
These decrease peripheral metabolism of L-dopa and improve absorption of L-dopa which decreases peripheral SEs
They don’t cross the BBB

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39
Q

Name the brands of the dopadecarboxylase inhibitors:

A

Carbidopa+ L-dopa= Co-careldopa (Sinemet®)
Benserazide+ L-dopa= Co-beneldopa (Madopar®)

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40
Q

Name 2 COMTi:

A

Entacapone
Tolcapone- rarely used due to risk of liver toxicity

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41
Q

Describe the SEs of entacapone:

A

Colours urine bright red/orange but this is harmless
Worsens SEs of L-dopa

42
Q

What is the function of COMTi?

A

Potentiates the effects of levodopa
Helps counteract fluctuations in plasma conc of L-dopa

43
Q

When are COMTi given?

A

Add on therapy in combo- not useful on their own

44
Q

What is the dosing of L-dopa?

A

Max of 800mg/ day in divided doses
-many can’t tolerate max dose, titrate benefits vs SEs

45
Q

What is a dosing schedule to help with fluctuation SEs of L-dopa but a negative of this too?

A

Small doses of L-dopa at increased frequency to decrease ‘peaks and troughs’ and dyskinesia but high tablet burden

46
Q

What are the counselling points for L-dopa?

A

Proteins inhibit the absorption, wait 30-60 mins after medication before eating- can eat a low protein snack like a cracker if nauseous
Brand specific
Manage underlying issues that affect absorption, iron supplements wait 2-3 hours as chelates form in GIT

47
Q

Name the different preparations of Levodopa:

A

Dispersible
Immediate release tab/cap
MR tab/cap
Intestinal gel for infusion

48
Q

Describe the use of dispersible L-dopa:

A

Quick onset- fast symptom relief
Admin via feeding tubes

49
Q

Describe the use of IR tabs/caps of L-dopa:

A

Slower onset
Prolonged action- up to 3 hours

50
Q

Describe the use of MR tabs caps of L-dopa:

A

Beneficial overnight
Slower onset
Substained action 4-5 hours

51
Q

Describe the use of the L-dopa intestinal gel:

A

Duodopa = co-careldopa
Admin via enteral tube

52
Q

Describe the benefits of dopamine receptor agonists as monotherapy compared to L-dopa:

A

Reduced (+increased time to) motor complications (less dyskinesia)
Can delay intro of L-dopa
Short plasma t1/2= 6-8 hours so TDS dosing

53
Q

Describe the disadvantages of dopamine receptor agonists as monotherapy compared to L-dopa:

A

Slightly poorer improvement in motor function
Possible greater neuro-psychiatric SEs
Older ergot derived are limited by SEs e.g N&V, thunderlance, fibrotic reactions of lung, heart valves= dangerous
Only be used if inadequate response to non-ergot derived options

54
Q

What are the SEs of non-ergot dopamine receptor agonists?

A

Better tolerated
Can sometimes cause thunderlance, compulsive behaviours e.g gambling, sex, eating

55
Q

Name non-ergot derived dopamine receptor agonists:

A

Ropinirole
Rotigotine- transdermal patch, useful when patients not able to take oral
Pramipexole

56
Q

Name ergot derived dopamine receptor agonists:

A

Bromocriptine
Cabergoline
Lisuride
Pergolide

57
Q

Who can impulse control disorders (ICD) affect?

A

Dopamine receptor agonist highest risk
As long as 4-5 years after starting treatment
More likely at younger age
More likely in male, smoking/ alcohol abuse

58
Q

Name some examples of ICD:

A

Compulsive gambling
Hypersexuality
Binge eating
Obsessive shopping

59
Q

What are the negative outcomes of ICD?

A

Can cause distress for patients and carers financial difficulties and even criminal convictions
May be difficult to recognise, particularly if patients conceal their behaviour from family/carers

60
Q

What should be the action if a PD patient is suspected of having ICD?

A

Gradually decrease any dopamine agonists
Monitor whether impulse control disorder improved and whether the person has any symptoms of dopamine receptor agonist withdrawal
Offer specialist cognitive behavioural therapy targeted at ICD behaviours if modification of dapaminergic therapy isn’t effective

61
Q

Name the monoamine oxidase B inhibitors (MAO-B):

A

Selegeline
Rasagiline

62
Q

What is the problem with selegeline?

A

Metabolised to amphetamine so causes excitement, anxiety and insomnia

63
Q

How do MAO-Bi work?

A

Enhances L-dopa action/over come ‘end of dose’ effect
MAO-B metabolises dopamine inhibition, so increases dopamine conc
Selectivity for B type receptors so do not interact with tyramine (cheese)

64
Q

When are MAO-Bi given?

A

Alone or as an adjunct

65
Q

What are the SEs for MAO-Bi?

A

Nausea
Postural hypotension
Dyskinesia
Confusion (elderly)

66
Q

How does amantadine work in PD?

A

MoA not fully understood
Increase dopamine levels (possibly by increasing dopamine release)
Mild benefit to symptoms

67
Q

When is amantadine given?

A

Only used as an adjuvant

68
Q

What is the problem and resolution of amantadine?

A

Efficacy diminishes within a few months of continuous treatment- slowly withdrawing and reintroducing the drug may prolong effectiveness

69
Q

What are the SEs of amantadine?

A

Psychological: hallucinations, delusions, paranoia, insomnia, anxiety, ICD
Sleep disturbances
GI: N&V, anorexia, weight loss, dry mouth
Hypotension
Palpitations

70
Q

Which initial treatment for PD offers the most improvement for motor symptoms?

A

Levodopa

71
Q

Which initial treatment for PD offers the most improvement for ADLs?

A

Levodopa

72
Q

Which initial treatment for PD offers the least motor complications?

A

Dopamine receptor agonists
MAO-Bi

73
Q

Which initial treatment for PD offers the least adverse events?

A

L-dopa
MAO-Bi

74
Q

Name the initial treatments in PD:

A

Ldopa
Dopamine r agonists
MAO-Bi

75
Q

Name the adjuvant therapies in PD:

A

Dopamine r agonists
MAO-Bi
COMTi
Amantadine

76
Q

Describe the adjuvant therapies affect on motor symptoms:

A

Dopamine r agonists- improvement
MAO-Bi- improvement
COMTi- improvement
Amantadine- no evidence of improvement

77
Q

Describe the adjuvant therapies affect on ADLs:

A

Dopamine r agonists- improvement
MAO-Bi- improvement
COMTi- improvement
Amantadine- no evidence of improvement

78
Q

Describe the adjuvant therapies affect on off time:

A

Dopamine r agonists- more off time
MAO-Bi- off time decreases
COMTi- off time decreases
Amantadine- no evidence report this

79
Q

Describe the adjuvant therapies affect on adverse events:

A

Dopamine r agonists- intermediate risk
MAO-Bi- fewer SEs
COMTi- more SEs
Amantadine- no studies report this

80
Q

Describe the adjuvant therapies on hallucinations:

A

Dopamine r agonists- more risk
MAO-Bi- lower risk
COMTi- lower risk
Amantadine- no studies report this

81
Q

Describe the significance of missing a dose of Parkinson’s medication:

A

Acute akinesia (inability to initiate movement)
Unable to communicate- more physically dependent on others
Loss of the ability to swallow, which increases risk of aspiration
Increase risk of falls, fractures
Neuroleptic- like malignant syndrome (very rare)

82
Q

Describe the symptoms of neuroleptic-like malignant syndrome:

A

Fever, marked rigidity (increase respiratory causing hypoventilation), altered consciousness, leucocytosis and elevated creatine kinase

83
Q

What is neuroleptic-like malignant syndrome caused by?

A

Caused by a sudden marked reduction in dopamine activity, either from withdrawal of dopaminergic agents or from blockage of dopamine receptors
More common in those with more severe PD symptoms or on high doses of Ldopa

84
Q

Name non-motor symptoms that can be treated in PD:

A

Mental health
Autonomic dysfunction
N&V
Pain
Sleep disturbance and daytime sleepiness
Pressure sores

85
Q

Describe mental health symptoms a PD patient can experience:

A

Depression, anxiety and apathy
Dementia and cognitive impairment
Impulse control and psychotic symptoms

86
Q

Describe autonomic dysfunction symptoms a PD patient can experience:

A

Constipation
Orthostatic (postural) hypotension
Excessive salivation and sweating
Bladder and sexual dysfunction

87
Q

What is the first line treatment to treat depression in PD?

A

SSRIs

88
Q

What is the treatment to help with dementia in PD?

A

Consider rivastigmine (licensed) or off label donepezil/ galantamine
Memantine last resort if these not tolerated

89
Q

What is the treatment for confusion/ hallucinations in PD?

A

Quetiapine (1st line)
Clozapine (2nd line)- high risk drug specialist initiation, regular monitoring

90
Q

What is the treatment for consitpation in PD?

A

Stimulant+ softener

91
Q

What is the treatment for postural hypotension in PD?

A

Midodrine (1st line)
Fludrocortisone

92
Q

What is the treatment for dysphagia in PD?

A

Medicines optimisation e.g dispersible tabs/ patches, build up drinks/ fluid thickener

93
Q

What is the treatment for salivation/ drooling in PD?

A

Glycopyrronium
Hyoscine

94
Q

What is the treatment for bladder dysfunction in PD?

A

Antimuscarinics e.g tolteradine, solefacin, oxybutinin

95
Q

What is the treatment for ED in PD?

A

PDE5i e.g sildenafil

96
Q

What is the treatment for N&V in PD?

A

Domperidone (1st line)
Consider cyclizine and ondansetron
NEVER metoclopramide/ prochlorperazine
Protein free snacks with L-dopa to decrease SEs e.g crackers

97
Q

What is the treatment for pain in PD?

A

Follow pain ladder
Consider SEs e.g drowsiness consitpation, PPIs with NSAIDs- PPI can increase fracture risk
Physiotherpay

98
Q

What is the treatment for sleep disturbances and daytime sleepiness in PD?

A

Sedatives- short term/occasional
Daytime sleepiness- modafinil- specialist use

99
Q

What is the treatment for pressure sores in PD?

A

Barrier creams
Change position every 2 hours
Pressure relieving mattresses and cushions

100
Q

What are some medicines management aspects for patients with PD:

A

Review all aspects of their care every 6-12 months
Prioritise med rec for parkinsons patients
Print medication timings on pharmacy labels
Avoid meds which worsen symptoms

101
Q

Name some OTC and POM meds which can worsen PD symptoms:

A

Sympathomimetics (e.g pseudoephedrine) with MAO-B inhibitors
OTC antihistamines
CCBs- occasional extrapyrimindal SEs, frequency unknown so need to monitor patients

102
Q

What are other considerations for patients with PD?

A

DVLA must be informed
Awareness of communications difficulties e.g quiet voice, slurred speech, decrease facial expressions
Encourage self admin and independence
Recommend cholecalciferol (vit D) as increase risk of osteoporosis

MPharm Y3S2 (22 decks)

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