W20 Parkinson's and Dementia (AG) Flashcards
(32 cards)
What is Parkinson’s disease?
- Parkinson’s disease (PD) is a chronic neurodegenerative disorder
- It is caused by the loss of dopamine-containing cells in the substantia nigra.
Risk Factors for Parkinsons’s disease? (5)
- Increasing age
- Male gender
- Head trauma
- Common genetic mutations (e.g. LRRK2, GBA, SNCA)
- Environmental toxin (e.g. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine [MPTP]) exposure
Symptoms – What are the Classical motor symptoms of idiopathic PD? (3)
other symptoms?
- Bradykinesia (slowness of movements, impared dexterity, delay in initiating movements, hypomimia-limits accurate expression of emotion)
- Parkinson’s tremor ( Involuntary tremor)
- Rigidity
Other symptoms:
Dystonia
Freezing
Postural instability
What are the Non-motor symptoms of PD?
- Constipation
- Sleep disorders (e.g. excessive daytime sleepiness, insomnia)
- Autonomic disturbances (e.g. urinary urgency, sweating, erectile dysfunction)
- Neuropsychiatric symptoms (e.g. anxiety, dementia, depression, hallucinations, delusions, mild memory and thinking difficulties)
- Speech and swallowing impairments (impaired swallowing, drooling, voice/speech disorder)
- Eye problem (e.g. excessive tearing)
- Pain (musculoskeletal pain)
- Fatigue
- Olfactory disturbance
Disease progression pattern- PD:
How many stages?
Stage 1: Mild symptoms that do not interfere with daily activities; for example, one sided tenors, posture, facial expressions
Stage 2: Symptoms worsen and daily tasks become more difficult and time-consuming. For example, tremors and rigidity affecting both sides of the body
Stage 3: Mid-stage of disease. Loss of balance and slowness of movement, resulting in increased falls. Still independent but simple activities such as dressing and eating may be difficult
Stage 4: Symptoms are severe and limiting. Movement may require a walker. Movement may require a walker. Patient needs help with daily activities and is unable to live alone
Stage 5: Stiffness in the legs may make it impossible to stand or walk. Patient requires a wheelchair or is bedridden. Around-the clock nursing needed. Patient may experience hallucinations and delusions. Important to manage both motor and non-motor symptoms.
Parkinson’s disease
Diagnosis:
- Prodromal phase lasting up to 20 years before diagnosis is emerging
- Differential diagnosis:
-Diseases that exhibit Parkinsonian symptoms but are not idiopathic PD include multiple system atrophy, progressive supranuclear
palsy, vascular PD and drug-induced Parkinsonism.
-Medications: older generation antipsychotics, antihistamines such as cinnarizine, methyldopa and antiemetics, such as metoclopramide — typically inhibit the actions of dopamine in the brain. - Diagnosis of PD is based on clinical presentation, as there is no reliable diagnostic test.
The need for multidisciplinary teams
(MDTs): PD
- GPs are not qualified to manage Parkinson’s meds= Consultant Neurologist
- Pharmacist- managemnt of motor and non-motor symptoms. Assess drug + food interactions
- PD Nurse specialist- clinical monitoring and medicines adjustment
- SALT- prevention exercises e.g. voice coaching
- Occ Physi- exercise, strengthening and stability
- Dieticians
Parkinson’s disease - Management
- Overall treatment is specific to the patient and the symptoms they experience.
- Symptoms can be variable from day to day or even hour to hour;
- Therefore, it is important that patients have a good understanding of their treatment, disease, coping mechanism, support system and regular reviews.
- Life expectancy can be normal.
- More advanced symptoms can lead to increased disability and poor health, which may make someone more vulnerable to complications (e.g. infection).
Pharmacological Management of Motor Symptoms: PD
3 drugs?
1.Administration of DA precursor (e.g. levodopa preparations such as co-careldopa);
2.Activation of DA receptors using DA agonists (e.g. ropinirole);
3.Enzyme inhibition to prevent the breakdown of DA (e.g.monoamine oxidase B inhibitors [MAO-B] and catechol-O-methyl transferase [COMT] inhibitors).
Parkinson’s disease - Levodopa Therapy
(DA precursors)
What is an example?
What is caused with long-term use?
Problems with missed dose?
- Levodopa + cabidopa or benserazide (dopa-decarboxylase inhibitors) (co-careldopa or co-beneldopa) to enable levodopa to cross the BBB and prevent break down of levodopa to DA in the gut (reducing side effects, such as N&V).
- Long-term use of levodopa can result in the patient experiencing dyskinesia and motor fluctuations (where the patient experiences ‘off-time’ periods, as the drug wears off and symptoms re-emerge). Also causes excessive daytime sleepiness.
- The short half-life and reducing duration of action make it important that patients get their medication on time every time.
- Late and missed doses contribute to risks of severe complications (e.g.** pneumonia and falls**)
Parkinson’s disease - DA agonists
- Preparations include M/R and I/R tablets (e.g. pramipexole and ropinirole), patches (rotigotine) and injections (apomorphine).
- There are two subclasses of DA agonists — ergoline and non-ergoline agonists — which both target DA D2-receptors.
1. Ergoline DA agonists, which include bromocriptine, pergolide, lisuride and cabergoline, are no longer routinely used in the treatment of PD because of adverse fibrotic^ reactions.
2. Non-ergoline DA agonists remain widely used and include ropinirole and pramipexole
^= thickening/scarring of tissue
Parkinson’s disease - DA agonists
What is the benefit of their use over levodopa?
When are Rotigotine or Apomorphine used?
Side effects?
▪ DA agonists may be less likely to cause dyskinesia and motor fluctuations than levodopa.
▪ Rotigotine is delivered transdermally via a patch, which can be particularly useful where patients have a high tablet burden or where patients have swallowing difficulties.
▪ Apomorphine is considered in advanced PD.
▪ Typical side effects include addictive gambling, hypersexuality, binge eating and obsessive shopping, somnolence, day-time sleepiness and hallucinations. Incidence increases with higher doses
Parkinson’s disease - DA agonists
Apomorphine S/C Injection:
Why is it given?
What to monitor?
Refractory motor fluctuations in Parkinson’s disease (‘off’ episodes) inadequately controlled by co-beneldopa or co-careldopa or other dopaminergics (for capable and motivated patients
Monitoring of patient parameters:
* Monitor hepatic, haemopoietic, renal, and cardiovascular function.
* With concomitant levodopa test initially and every 6 months for haemolytic anaemia and thrombocytopenia (development calls for specialist haematological care with dose reduction and possible discontinuation
Parkinson’s disease - COMTIs:
What is used and why?
- The inhibition of COMT prevents peripheral breakdown of levodopa, allowing more levodopa to reach the brain and prolonging the effect of levodopa dosing.
- As a result, concurrent levodopa doses need to be reviewed and possibly reduced by up to 30%.
- The COMT inhibitor entacapone is usually taken with each levodopa dose and is available alone or as a combination product with levodopa and carbidopa (which can be helpful in reducing tablet burden).
- An alternative is opicapone, which is taken just OD.
Parkinson’s disease – Adjuvant therapy e.g. Glutamate Antagonists
Example?
Why are they used?
▪ Glutamate antagonists, such as amantadine, are generally used to reduce dyskinesia caused by levodopa therapy.
▪ They can be used in all stages of PD, but are often prescribed when alternative strategies have not effectively managed motor complications.
dyskinesia= uncontrolled, involuntary movement
Parkinson’s disease - Monoamine oxidase B inhibitors:
What is their moA?
What are cautioned to take alongside MOABs and why?
▪ MAO-B inhibitors increase the length of time DA is active in the brain by preventing it from being broken down.
▪ Rasagiline and selegiline can be prescribed in early disease as monotherapy, and any can be used in combination with other treatments later in the disease course.
▪ Concomitant antidepressants are cautioned with MAO-B inhibitors because of the risk of serotonin syndrome.
▪ Hypertension is common when high-dose selegiline is taken with tyramine-rich foods
PD
Drug management non-motor symptoms
Day time sleepiness and sudden onset of sleep:
▪ Sleep hygiene
▪ Adjust medications
▪ Modafinil
▪ DVLA needs to be informed and patient
advised not to drive
Psychotic symptoms:
▪ Quetiapine for hallucinations and delusions
▪ Olanzapine, risperidone, phenothiazines and butyrophenones, should be avoided as they can worsen motor features of PD by blocking DA receptors
Nocturnal akinesia:
▪ levodopa or DA-receptor agonists or rotigotine
Constipation:
▪ Macrogol
▪ A high-fibre diet, exercise (if possible) and adequate fluid intake
Rapid eye movement sleep behaviour disorder
▪ Clonazepam or melatonin
Drooling of saliva
▪ glycopyrronium bromide
Parkinson’s disease dementia
▪ An acetylcholinesterase inhibitor- donepezil, rivastigmine, galantamine
Postural hypotension
▪ Midodrine or fludrocortisone (consider cardiac risks)
N&V
▪ Preferably no drugs
▪ Advice on a toast or a dry biscuit to take before taking levodopa for example.
Advanced Parkinson’s Disease:
What drug is used to treat non-motor symptoms?
Apomorphine (DA)
▪ N&V- domperidone can be used.Preferably no antiemetic. Advise on eating a dry biscuit or toast before drug administration.
▪ Assessment of cardiac risk factors and ECG monitoring due to risk of serious arrhythmia due to QT prolongation
▪ Domperidone restricted in those weighing <35 Kg
Impulse control disorders - Apomorphine
▪ Compulsive gambling, hypersexuality, binge eating or obsessive shopping can develop in patients on dopaminergic therapy. Patients should be informed about the risk of impulse control disorders
Quiz 1
1. How would you transfer a patient from a levodopa/dopa-decarboxylase inhibitor preparation to another?
2. What would be the implications of discontinuing co-careldopa abruptly?
3. Counsel patients on the use of co-beneldopa dispersible tablets
4. Counsel patients on the use of rotigotine patches
5. What are the equivalent strengths of pramipexole (base) in terms of 2mg pramipexole dihydrochloride monohydrate (salt) for immediate-release preparations?
- When transferring patients from another levodopa/dopa-decarboxylase inhibitor preparation, the previous preparation should be discontinued at least 12 hours before.
- Abrupt withdrawal may increase the risk of neuroleptic malignant syndrome and rhabdomyolysis.
- Dispersible tablets can be dispersed in water or orange squash (NOT orange juice).
Dispersible tablets, capsules, and modified-release capsules should be taken 30 minutes before or 1 hour after meals.
If undesirable GI effects occur, this may be controlled by taking doses with a low-protein snack or liquid - Avoid exposure of patch to heat; remove patch (aluminium-containing) before magnetic resonance imaging or cardioversion.
Manufacturer advises apply patch to clean, dry, intact, healthy and non-irritated skin on torso, thigh, hip, shoulder or upper arm by pressing the patch firmly against the skin for about 30 seconds.
Patches should be removed after 24 hours and the replacement patch applied on a different area (avoid using the same area for 14 days)—consult product literature for further information - 700 micrograms base ≡ 1 mg salt.
Therefore
1400 micrograms base ≡ 2 mg salt
What is Dementia? definition?
Dementia is a progressive clinical syndrome characterised by a range of cognitive and
behavioural symptoms that can include memory loss, problems with reasoning and
communication, a change in personality, and a reduced ability to carry out daily
activities such as washing or dressing
DEMENTIA
Cognitive Symptoms?
Non-Cognitive symptoms?
Dementia is irreversible, progressive decline and impairment of more than one aspect
of higher brain function (concentration, memory, language, personality, emotion).
This occurs without impairment of consciousness.
Cognitive Symptoms:
Memory loss
Lack of concentration
Disorientated
Difficulty with speech
Non-Cognitive
Symptoms:
Agitation
Aggression
Distress
Psychosis
Dementia - Diagnosis
How can a diagnosis be made?
Usually made clinically from the history (patient and collateral), cognitive tests (6-CIT, GPCOG, 7-minute screen, etc), and formal neuropsychological assessment
What are the clinical features of the different Dementias? (4)
- Alzheimer’s dementia:
* Develops after the age of 60
* Memory loss, with evidence of varying changes in planning, reasoning, speech and orientation. - Vascular dementia:
*Cognitive impairment
* Patients should be screened for depression and for signs of psychomotor retardation - Lewy Body dementia:
* Involves visual hallucinations and Parkinson-like symptoms.
* Problems multitasking and performing complex cognitive actions.
* Sleep disorders and fluctuations in cognitive ability. - Frontotemporal dementia:
* Develops in <65s
* Behavioural (decline in interpersonal skills, changes in food preferences)
* Semantic (Not recognising words, familiar faces)
* Non-Fluent (speech apraxia = poor articulation)
How to communicate with dementia patients?
- Be patient.
- Minimise distractions
- Be consistent
- Keep the conversation simple
- Non-verbal communication
- Avoid a large volume of direct questions
- Validate the person’s feelings and re-direct
them rather than trying to re-orient them - Physical touch
- Dealing with challenging behaviours
(wandering, agitation, paranoia, disinhibition)
-V – Validate
-E – Emotional connection
-R – Reassurance
-A - Activity
