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MPharm Y3S2 > Clinical CNS Parkinson's > Flashcards

Clinical CNS Parkinson's Flashcards

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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
Describe how viral illnesses can cause Parkinsonism:
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
26
Describe the diagnosis for PD:
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
27
Name and describe the neurological examinations that occur for a PD diagnosis:
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
28
What are the steps in diagnosing PD?
Step 1: Diagnosis of parkinsonian syndrome- motor symptoms Step 2: Exclusion criteria Step 3: Supportive criteria
29
What is the first line treatment in PD with motor symptoms?
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
30
What is the adjuvant therapy in PD with motor symptoms?
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
31
Describe the use of L-dopa in PD:
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
32
When should you start L-dopa?
Different for every patient e.g older patient may want to start asap but younger may want to start it later
33
What are the unwanted SEs of L-dopa?
Dyskinesia (involuntary movements) Fluctuations in clincal state Acute SEs
34
Describe the dyskinesia SE for L-dopa:
From 2 years of starting (50% of patients by year 5) Affects face, arm and trunk (limbs)
35
Describe the fluctuations in clinical state SE for L-dopa:
'On-off' phenomena (bradykinesia/ rigidity suddenly worsen then better) Wearing off effect (end of dose deterioration) Freezing
36
What are possible solutions for PD patients when they get symptoms due to wearing off their medication?
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
37
Describe the acute SEs for L-dopa:
Nausea and anorexia Hypotension Sleep disturbances including sudden onset of sleep implications for driving Psychological effects- anxiety/ depression, schizophrenia symptoms
38
Name inhibitors that is given with L-dopa to inhibit the metabolism and why?
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
39
Name the brands of the dopadecarboxylase inhibitors:
Carbidopa+ L-dopa= Co-careldopa (Sinemet®) Benserazide+ L-dopa= Co-beneldopa (Madopar®)
40
Name 2 COMTi:
Entacapone Tolcapone- rarely used due to risk of liver toxicity
41
Describe the SEs of entacapone:
Colours urine bright red/orange but this is harmless Worsens SEs of L-dopa
42
What is the function of COMTi?
Potentiates the effects of levodopa Helps counteract fluctuations in plasma conc of L-dopa
43
When are COMTi given?
Add on therapy in combo- not useful on their own
44
What is the dosing of L-dopa?
Max of 800mg/ day in divided doses -many can't tolerate max dose, titrate benefits vs SEs
45
What is a dosing schedule to help with fluctuation SEs of L-dopa but a negative of this too?
Small doses of L-dopa at increased frequency to decrease 'peaks and troughs' and dyskinesia but high tablet burden
46
What are the counselling points for L-dopa?
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
Name the different preparations of Levodopa:
Dispersible Immediate release tab/cap MR tab/cap Intestinal gel for infusion
48
Describe the use of dispersible L-dopa:
Quick onset- fast symptom relief Admin via feeding tubes
49
Describe the use of IR tabs/caps of L-dopa:
Slower onset Prolonged action- up to 3 hours
50
Describe the use of MR tabs caps of L-dopa:
Beneficial overnight Slower onset Substained action 4-5 hours
51
Describe the use of the L-dopa intestinal gel:
Duodopa = co-careldopa Admin via enteral tube
52
Describe the benefits of dopamine receptor agonists as monotherapy compared to L-dopa:
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
Describe the disadvantages of dopamine receptor agonists as monotherapy compared to L-dopa:
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
What are the SEs of non-ergot dopamine receptor agonists?
Better tolerated Can sometimes cause thunderlance, compulsive behaviours e.g gambling, sex, eating
55
Name non-ergot derived dopamine receptor agonists:
Ropinirole Rotigotine- transdermal patch, useful when patients not able to take oral Pramipexole
56
Name ergot derived dopamine receptor agonists:
Bromocriptine Cabergoline Lisuride Pergolide
57
Who can impulse control disorders (ICD) affect?
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
Name some examples of ICD:
Compulsive gambling Hypersexuality Binge eating Obsessive shopping
59
What are the negative outcomes of ICD?
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
What should be the action if a PD patient is suspected of having ICD?
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
Name the monoamine oxidase B inhibitors (MAO-B):
Selegeline Rasagiline
62
What is the problem with selegeline?
Metabolised to amphetamine so causes excitement, anxiety and insomnia
63
How do MAO-Bi work?
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
When are MAO-Bi given?
Alone or as an adjunct
65
What are the SEs for MAO-Bi?
Nausea Postural hypotension Dyskinesia Confusion (elderly)
66
How does amantadine work in PD?
MoA not fully understood Increase dopamine levels (possibly by increasing dopamine release) Mild benefit to symptoms
67
When is amantadine given?
Only used as an adjuvant
68
What is the problem and resolution of amantadine?
Efficacy diminishes within a few months of continuous treatment- slowly withdrawing and reintroducing the drug may prolong effectiveness
69
What are the SEs of amantadine?
Psychological: hallucinations, delusions, paranoia, insomnia, anxiety, ICD Sleep disturbances GI: N&V, anorexia, weight loss, dry mouth Hypotension Palpitations
70
Which initial treatment for PD offers the most improvement for motor symptoms?
Levodopa
71
Which initial treatment for PD offers the most improvement for ADLs?
Levodopa
72
Which initial treatment for PD offers the least motor complications?
Dopamine receptor agonists MAO-Bi
73
Which initial treatment for PD offers the least adverse events?
L-dopa MAO-Bi
74
Name the initial treatments in PD:
Ldopa Dopamine r agonists MAO-Bi
75
Name the adjuvant therapies in PD:
Dopamine r agonists MAO-Bi COMTi Amantadine
76
Describe the adjuvant therapies affect on motor symptoms:
Dopamine r agonists- improvement MAO-Bi- improvement COMTi- improvement Amantadine- no evidence of improvement
77
Describe the adjuvant therapies affect on ADLs:
Dopamine r agonists- improvement MAO-Bi- improvement COMTi- improvement Amantadine- no evidence of improvement
78
Describe the adjuvant therapies affect on off time:
Dopamine r agonists- more off time MAO-Bi- off time decreases COMTi- off time decreases Amantadine- no evidence report this
79
Describe the adjuvant therapies affect on adverse events:
Dopamine r agonists- intermediate risk MAO-Bi- fewer SEs COMTi- more SEs Amantadine- no studies report this
80
Describe the adjuvant therapies on hallucinations:
Dopamine r agonists- more risk MAO-Bi- lower risk COMTi- lower risk Amantadine- no studies report this
81
Describe the significance of missing a dose of Parkinson's medication:
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
Describe the symptoms of neuroleptic-like malignant syndrome:
Fever, marked rigidity (increase respiratory causing hypoventilation), altered consciousness, leucocytosis and elevated creatine kinase
83
What is neuroleptic-like malignant syndrome caused by?
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
Name non-motor symptoms that can be treated in PD:
Mental health Autonomic dysfunction N&V Pain Sleep disturbance and daytime sleepiness Pressure sores
85
Describe mental health symptoms a PD patient can experience:
Depression, anxiety and apathy Dementia and cognitive impairment Impulse control and psychotic symptoms
86
Describe autonomic dysfunction symptoms a PD patient can experience:
Constipation Orthostatic (postural) hypotension Excessive salivation and sweating Bladder and sexual dysfunction
87
What is the first line treatment to treat depression in PD?
SSRIs
88
What is the treatment to help with dementia in PD?
Consider rivastigmine (licensed) or off label donepezil/ galantamine Memantine last resort if these not tolerated
89
What is the treatment for confusion/ hallucinations in PD?
Quetiapine (1st line) Clozapine (2nd line)- high risk drug specialist initiation, regular monitoring
90
What is the treatment for consitpation in PD?
Stimulant+ softener
91
What is the treatment for postural hypotension in PD?
Midodrine (1st line) Fludrocortisone
92
What is the treatment for dysphagia in PD?
Medicines optimisation e.g dispersible tabs/ patches, build up drinks/ fluid thickener
93
What is the treatment for salivation/ drooling in PD?
Glycopyrronium Hyoscine
94
What is the treatment for bladder dysfunction in PD?
Antimuscarinics e.g tolteradine, solefacin, oxybutinin
95
What is the treatment for ED in PD?
PDE5i e.g sildenafil
96
What is the treatment for N&V in PD?
Domperidone (1st line) Consider cyclizine and ondansetron NEVER metoclopramide/ prochlorperazine Protein free snacks with L-dopa to decrease SEs e.g crackers
97
What is the treatment for pain in PD?
Follow pain ladder Consider SEs e.g drowsiness consitpation, PPIs with NSAIDs- PPI can increase fracture risk Physiotherpay
98
What is the treatment for sleep disturbances and daytime sleepiness in PD?
Sedatives- short term/occasional Daytime sleepiness- modafinil- specialist use
99
What is the treatment for pressure sores in PD?
Barrier creams Change position every 2 hours Pressure relieving mattresses and cushions
100
What are some medicines management aspects for patients with PD:
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
Name some OTC and POM meds which can worsen PD symptoms:
Sympathomimetics (e.g pseudoephedrine) with MAO-B inhibitors OTC antihistamines CCBs- occasional extrapyrimindal SEs, frequency unknown so need to monitor patients
102
What are other considerations for patients with PD?
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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