Download Free Medical Idiopathic parkinsons disease (IPD) PowerPoint Presentation

Idiopathic parkinsons disease (IPD) PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Neurology, which is titled "Idiopathic parkinson’s disease (IPD)", to know about the Definition, Aetiology, Pathology, Clinical features, Investigations, Differential diagnoses, and Management of Idiopathic parkinson’s disease (IPD).

Tags : Neurology, Idiopathic parkinson’s disease, IPD, Definition, Aetiology, Pathology, Clinical features, Investigations, Differential diagnoses, Management

Published on : Aug 18, 2021 | Views : 2033 | Downloads : 7

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Idiopathic parkinson’s disease (IPD) Dr Sabrina Akhtar
Slide 2-

Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
Slide 3-

Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
Slide 4-

Defining IPD Named after James Parkinson who published 'An Essay on the Shaking Palsy' in 1817, which established Parkinson’s as a recognised medical condition. He studied at the London Hospital Medical College, qualifying as a surgeon in 1784 when he was 29.
Slide 5-

Defining IPD -Degenerative, progressive disease affecting the basal ganglia. Movement disorders: 1) Akinetic-rigid syndromes - Slowed movement. - Increased tone. -> IPD, drug-induced parkinsonism, multiple systems atrophy, progressive supranuclear palsy. 2) Dyskinesias -Added, uncontrollable movements. -> Essential tremor, chorea, myoclonus, tics.
Slide 6-

Defining IPD
Slide 7-

Defining IPD Annual incidence- 0.2/1000. Prevalence- 1/500 (127 000 people in the UK). Tends to affect ≥50 years. 1/20 is under the age of 20 years. Incidence and prevalence increase with age. Equal sex incidence.
Slide 8-

Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
Slide 9-

Aetiology Unknown aetiology. Several theories: Nicotine- IPD is less prevalent in smokers than lifelong abstainers. MPTP- caused severe parkinsonism in young drug abusers. Genetic factors- clustering of early-onset PD in some families.
Slide 10-

Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
Slide 11-

Pathology Basal ganglia: Group of nuclei in the brain situated at the base of the forebrain (striatum, globus pallidus, substantia nigra [SN], nucleus accumbens, subthalamic nucleus). Associated with voluntary motor control, procedural learning, eye movements, cognitive and emotional functions.
Slide 12-

Pathology
Slide 13-

Pathology
Slide 14-

Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
Slide 15-

Clinical features
Slide 16-

Clinical features
Slide 17-

Clinical features
Slide 18-

Clinical features
Slide 19-

Clinical features
Slide 20-

Clinical features Gait: Stooping Slow to initiate walking Shortened stride Rapid small steps (shuffling) Tendency to run (festinating) Reduced arm swing Impaired balance on turning Falls common in later stages. Parkinson’s gait
Slide 21-

Clinical features Speech -Monotone tremulous, slurring dysarthria. -Soft, rapid, indistinct. Cognitive -Cognitive impairment in 1/3 of patients (loss of executive functions including planning/decision-making/controlling emotions). -Depression.
Slide 22-

Clinical features GI/others -Constipation/heartburn/dribbling/ dysphagia/weight loss. -Greasy skin. -Micrographia.
Slide 23-

Clinical features
Slide 24-

Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
Slide 25-

Investigations Clinical diagnosis. <50 years: Test for Wilson’s disease. CT head scan if: - Pyramidal/cerebellar/autonomic involvement. - Diagnosis is in doubt.
Slide 26-

Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
Slide 27-

Differential diagnoses Multiple systems atrophy Progressive supranuclear palsy Lewy body dementia Drug-induced parkinsonism Vascular parkinsonism
Slide 28-

ppt slide no 28 content not found
Slide 29-

Objectives Definition Aetiology Pathology Clinical features Investigations Differential diagnoses Management
Slide 30-

Management Medical: Levodopa + peripheral decarboxylase inhibitor (E.g. Carbidopa, Benserazide). -Levodopa: Precursor of dopamine stimulates remaining neurons to produce more dopamine. -Decarboxylase inhibitor: Prevents peripheral decarboxylation to dopamine and .:. peripheral SE’s.
Slide 31-

Management Side effects of levodopa: -N&V -Confusion -Visual hallucinations -Delusions -Chorea LT effects: -Levodopa-induced involuntary movements. -Gradually ineffective after several years. -Episodes of immobility (freezing). THEREFORE drugs are avoided until clinically necessary (significant disability) because of delayed unwanted effects.
Slide 32-

Management Other medical treatment options: -Dopamine receptor agonists (Bromocriptine/Cabergoline). -Amantadine. -Rivastigmine (cognitive changes). -Antioxidant compounds (Vitamins C & E- possible neuroprotective agents).
Slide 33-

Management Surgical -Stereotactic thalamotomy- temporary improvement of symptoms. Physiotherapy Reduces rigidity & corrects abnormal posture. Speech therapy -Dysarthria/dysphonia. Neuropsychiatric - SSRI’s for depression.
Slide 34-

Management Natural history: Slowly progressive (10-15 years). Bradykinesia & tremor worsen. Late deterioration despite Levodopa Rx occurs in 1/3-1/2 of patients after 3-5 years. This includes the ‘on-off’ phenomenon. Patient’s c/o limb & joint discomfort.
Slide 35-

Management Prognosis -Partly related to age of onset e.g. if symptoms start in middle life  disease likely to shorten lifespan (complications of immobility & tendency to fall). Onset >70 years of age unlikely to shorten life/become severe.
Slide 36-

Summary IPD is the most common cause of parkinsonism. Degenerative, progressive disease affecting the basal ganglia. Classical features include tremor, rigidity and bradykinesia. Mainstay of treatment is with levodopa & a PDI. Treatment is delayed until clinically necessary because of unwanted delayed effects of levodopa. Multi-disciplinary approach to management.
Slide 37-

Thank you!  Questions?