Download Free Medical Parkinsons Disease PowerPoint Presentation

Parkinsons Disease PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Parkinson’s Disease” by Harald Bjorndalen.

This medical PowerPoint presentation is about Parkinsons disease (PD), a progressive neurological disorder that affects movement. It is caused by the degeneration of dopamine-producing neurons in the brain, which leads to a shortage of dopamine and results in symptoms such as tremors, rigidity, and slow movements.

While there is no cure for PD, there are several treatment options that can help manage the symptoms and improve quality of life. These treatments can include medication, surgery, and lifestyle changes.

Medications: There are several classes of medications used to treat PD, including levodopa, dopamine agonists, MAO-B inhibitors, and anticholinergics. Levodopa is the most effective medication and is converted into dopamine in the brain. Dopamine agonists mimic the effects of dopamine and can be used alone or in combination with levodopa. MAO-B inhibitors and anticholinergics can also help manage symptoms.

Surgery: Deep brain stimulation (DBS) is a surgical procedure that can help manage symptoms in people with PD. DBS involves implanting electrodes in specific areas of the brain, which can be controlled with an external device. This can help reduce tremors, stiffness, and other symptoms.

Lifestyle changes: Regular exercise, physical therapy, and occupational therapy can help manage symptoms and improve mobility. A balanced diet can also be beneficial, as can avoiding certain medications and substances that can worsen symptoms.

Overall, the best treatment plan for PD will depend on the individuals symptoms, stage of the disease, and other factors. It is important to work with a healthcare provider to develop a personalized treatment plan and regularly adjust it as needed.

Tags : Parkinson’s disease, neurodegenerative disorder, dopamine-producing cells, brain, Deep brain stimulation, Neurology, Neurology PowerPoint presentation

Published on : Jun 20, 2023 | Views : 3611 | Downloads : 5

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Parkinson’s Disease Harald Bjorndalen Adapted from lecture by Dr Zoe Campbell (Medical SpR)
Slide 2-

Understand difference between Parkinson’s Disease and Parkinsonism Describe clinical features of Parkinson’s disease Describe basic management of parkinson’s disease Learning Outcomes
Slide 3-

Case Pathophysiology Definition Clinical features Investigations Management Prognosis Outline
Slide 4-

Clinical scenario A 64 year old man attends his GP after his wife persuaded him. For the last 6 months he has noticed that he is slowing down. It takes him a long time to do simple tasks like getting dressed. His hands are shaking all the time, more so on the right. His wife has noticed a change in his gait saying he shuffles when he walks. He has no past medical history of notes and is on no regular medication and has no known allergies. On examination he has a blank staring expression and marked rigidity of his limbs, more so on the right. He has resting pill rolling tremor. His gait is shuffling and festinant.
Slide 5-

What are your differentials for this gentleman? How would you investigate this man? How would you manage this gentleman? What are the stages of managing Parkinson’s Disease? What are the Parkinson’s plus syndromes? What drugs can cause Parkinsonism?
Slide 6-

Parkinson’s Disease
Slide 7-

Loss of dopaminergic neurones in the substantia nigra and appearance of eosiniphilic inclusion bodies (Lewy bodies) Parkinson’s - Pathophysiology
Slide 8-

Classic TRIAD: BRADYKINESIA / slowness RIGIDITY / stiffness / increased tone TREMOR / pill rolling / 4-6 Hz /resting Postural instability Parkinson’s - History
Slide 9-

Neurodegenerative disease of the dopamine generating neurones in the substantia nigra, characterized by bradykinesia, rigidity, tremor, and postural instability Definition
Slide 10-

What is PARKINSONISM? What are the causes? Parkinson’s
Slide 11-

Neurological syndrome characterised by tremor, bradykinesia and rigidity. Causes DRUGS – Anti psychotics, metaclopramide, TCA, MPTP Vascular disease Parkinson plus syndromes (multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration, Lewy-body dementia) Trauma Parkinsonism
Slide 12-

Onset - gradual Tremor – at rest, usually first noticed in the hands Stiffness and slowness of movement. Difficulty initiating movements (e.g. getting out of chair, turning in bed) Falls – Not usually frequent early on Smaller hand writing Parkinson's - History
Slide 13-

Anxiety/depression Sleep disturbance Postural hypotension Sweating Constipation Drooling Incontinence Sexual dysfunction Parkinson’s - History
Slide 14-

Symmetry Lower body involvement Poor response to levodopa Early falls / postural instability Early autonomic disturbance (sexual, bladder, postural hypotension) Early eye movement disorders Early dementia Early dysarthria Parkinson's – Red Flags
Slide 15-

Cranial nerves Upper limb Lower limb Gait Function Parkinson's - Examination
Slide 16-

Face – expressionless / mask like / reduced blinking Parkinson's - Examination
Slide 17-

Speech Monotonous Tremulous slurring dysarthria (due to akinesia, tremor and rigidity of bulbar area) Dribbling and drooling Parkinson’s - Examination
Slide 18-

Tremor Worse at rest Asymmetrical Parkinson’s - Examination
Slide 19-

Increased tone / cogwheeling Power normal Reflexes normal Sensation normal Coordination normal (but might be slow)
Slide 20-

Gait Stooped posture Gunslinger/Hands over hernias Shuffling Reduced arm swing Difficulty turning (axial rigidity) Parkinson’s - Examination
Slide 21-

Rapidly open and close hands Functional tasks Get the patient to write a sentence Draw a spiral AMT Lying / standing BP Parkinson’s - Examination
Slide 22-

Diagnosis is CLINICAL Bedside tests: Levodopa trial. Routine bloods CT and MRI usually normal but may exclude other causes of parkinsonism PET / SPECT scans can be used to measure dopaminergic function in basal ganglia. Parkinson’s - Investigation
Slide 23-

MDT: Physios OT Neurologist GP PD nurse Support societies Palliative care in the late stages Parkinson’s - Management
Slide 24-

Medical: Dopamine agonists e.g. ropinirole, bromocriptine MAO inhibitors e.g. rasagiline Levodopa + decarboxylase inhibitor COMT e.g. Entacapone Continuous dopamine therapy – Apomorphine (syringe driver) or Duodopa (Intrajejunal infusion of levodopa gel) Supportive medication e.g. Baclofen, antidepressants Parkinson’s- Management
Slide 25-

ppt slide no 25 content not found
Slide 26-

Depression, psychosis Dementia Sleep disorders Restless legs syndrome Periodic limb movements of sleep REM sleep behaviour disorder Falls Autonomic disturbance urinary dysfunction weight loss, dysphagia constipation erectile dysfunction orthostatic hypotension excessive sweating sialorrhoea Non-motor symptoms in PD clonazepam movicol Citalopram Quetiapine, clozapine Acetylcholinesterase inhibitors Oxybutynin, tolterodine
Slide 27-

Guidelines for drug management of PD Significant functional disability Disease progression Dopamine agonist Add levodopa (max 600mg/day) Motor complications develop Add DA or entacapone MAO-B inhibitor Add entacapone or DA Levodopa (max 600mg/day) Switch to tolcapone if entacapone fails Add MAO-B inhibitor if not already given Add amantadine for dyskinesia Severe motor complications Consider apomorphine, Duodopa, DBS
Slide 28-

Parkinson’s - Management Surgical: Deep brain stimulation A lead is implanted into the target area (brainstem) This lead connects to a implantable pulse generator Which connects to a device in the subclavian area of the chest Device produces mono polar or bi polar electrical stimulation to control symptoms
Slide 29-

Parkinson’s - Management
Slide 30-

74 year old Diagnosed with PD, right sided tremor, bradykinesia/rigidity-all mild L-dopa started after 10 months as symptoms worsened, problems with stairs Started on sinemet 62.5mg od then incresed to tds over 1 week. No response after 2 weeks What next? Case History 2
Slide 31-

Dose incresed to 125mg tds with good response Stable over 2 years then mobility worsened and patient getting slow and stiff before next drug dose What next? Increase sinemet to qds (OR add entacapone) Over next 3 years, dose increased to sinemet 250, 125, 250, 125 plus sinemet CR nocte 3 years after increase- fluctuations in response- drugs not always helping him switch on, extra movements an hour after taking his medications, switched off prior to his next dose What next?
Slide 32-

Sinemet decreased to 125 qds plus CR nocte Entacapone added No improvement, slightly worse over 6 months What next? Ropinirole added Dose slowly increased over 8 months (79 yrs old), hallucinations, mild cognitive decline Ropinirole decreased, symptoms worsened Quetiapine added Sinemet levels maintained
Slide 33-

Surgical: Deep brain stimulation A lead is implanted into the target area (brainstem) This lead connects to a implantable pulse generator Which connects to a device in the subclavian area of the chest Device produces mono-polar or bi-polar electrical stimulation to control symptoms Parkinson’s - Management
Slide 34-

MDT: Physio OT Neurologist GP Support societies Palliative care in the late stages Parkinson’s - Management
Slide 35-

Progression variable Usually the course is over 10-15 years Death from pneumonia Parkinson’s - Prognosis
Slide 36-

- Sam AH, Teo JTH, Rapid Medicine, Wiley-Blackwell 2010 - BMJ learning module: Parkinson's disease - initial assessment and referral - Lecture by Zoe Campell, Warwick Hospital, 2012 - SADH lecture by Naghme Adab, Management and treatment of Parkinson’s Disease, 2012 References/Further reading