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Parkinson’s
Disease
PRESENTED BY: Okumu Jeremiah Valley
 Definition and causes
 Epidemiology and predisposing factors
 Pathophysiology
 Signs and symptoms
 Management
 Applied pharmacology
PARKINSON'S DISEASE (PD)
CLINICAL OVERVIEW.
Progressive Neurodegenerative disorder
of the dopaminergic neurones in the
substantia nigra.
Parkinsonism is a clinical syndrome
consisting of four cardinal features:
 Bradykinesia (slowness and poverty of
movement)
 Muscular rigidity
 Resting tremor (which usually abates
during voluntary movement)
 Impairment of postural balance leading to
disturbances of gait and falling .
 Most common neurologic disorder affecting
approximately 1% of the population of
individuals above 60years of age
 7.5 million people world wide
 The most common cause of parkinsonism is
idiopathic PD, first described by James
Parkinson in 1817 as paralysis agitans, or
the "shaking palsy." The pathological
hallmark of PD is a loss of the pigmented,
dopaminergic neurons of the substantia
nigra pars compacta, with the appearance of
intracellular inclusions known as Lewy
bodies.
 Progressive loss of dopamine-containing
neurons is a feature of normal aging;
however, most people do not lose the 70% to
80% of dopaminergic neurons required to
cause symptomatic PD.
 Genetic
factors(PARK2/7,PIN
K1)
 Environmental
factors - manganese
and pesticides
 Drugs -
antipsychotics
(clozapine)
 Cerebrovascular
disease (stroke)
 Smoking
 Coffee
 The primary deficit in PD is a loss of the
neurons in the substantia nigra pars
compacta that provide dopaminergic
innervation to the striatum (caudate and
putamen).since dopamine facilitates the
inhibiton on a wide range of motor activities,
release of this inhibiton causes in
appropriate activation of these motor
activities
 The presence of lewy bodies
 Stage 1 - Mild symptoms such as tremors
 Stage 2 - Symptoms are bilateral
 Stage 3 - Inability to walk straight or
stand
 Stage 4 - Rigidity and bradykinesia
 Stage 5 - Unable to take care of themselves
and requires a contant one on one nursing
care
 Cardinal Features
-Resting tremors
-Rigidity
-Bradykinesia
-Postural instability
 Other features
-Hypomimia
-Dysphagia
-Hypohonia
-Shuffling gait
-Festinations
 Medical
-Gene therapy
-Dietary consideration
-Deep brain stimulation
-Neural transplantation
-Speech therapy
-Exercise and physical therapy
-Pharmarcological therapy
 Nursing
-Assessment
1. •Do you have leg or arm stiffness?
2. •Have you experienced any irregular jerking of
your arms or legs
3. • Have you ever been “frozen” or rooted to the
spot and unable to move
4. • What specific activities do you have difficulty
doing?
 During this assessment, the nurse observes
the patient for quality of speech, loss of facial
expression, swallowing deficits,tremors
 slowness of movement, weakness, forward
posture, rigidity and evidence of mental
confusion
 Diagnosis
1. • Impaired physical mobility related to muscle
rigidity and motor weakness
2. • Self-care deficits (feeding, dressing, hygiene, and
toileting) related to tremor and motor disturbance
3. • Imbalanced nutrition, less than body
requirements, related to tremor, slowness in
eating, difficulty in chewing and swallowing
4. • Impaired verbal communication related to
decreased speech volume, slowness of speech,
inability to move facial muscles
 Planning and goals
 Improving functional mobility
 Maintaining independence in activities of
daily living
 Achieving adequate bowel elimination,
attaining and maintaining acceptable
nutritional status
 Achieving effective communication
 Interventions
Mobility - range-of-motion exercises
promote joint flexibility
- Warm baths and massage to relax
muscles
Self care - Teaching, supporting and
encouraging the patient during activities
of daily living promote self-care
Nutrition - Monitoring weight on a weekly basis
indicates whether caloric intake is adequate
- Nasogastric tube maybe necessary as
the disease progresses
Communication - A speech therapist may be
helpful in designing speech improvement
exercises and assisting the family and health care
personnel to develop and use a method of
communication to meet the patient’s needs
 Dopamine Agonists
- levodopa combined with a peripheral
decarboxlase inhibitor e.g cardidopa
 Anticholinergics
- benztropine mesylate for treatment of motor
symptoms
 MAO-Inhibitors
- selegiline block the breakdown of dopamine
 Acetylcholinesterase inhibitors (central)
-Donepazil treatment of dimentia
 COMT Inhibitors
-Tolcapone inhibit COMT the major catecholamine
degrader
 Medscape,wikipedia,katzung.
 O.J

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Parkinsons disease o.j

  • 2.  Definition and causes  Epidemiology and predisposing factors  Pathophysiology  Signs and symptoms  Management  Applied pharmacology
  • 3. PARKINSON'S DISEASE (PD) CLINICAL OVERVIEW. Progressive Neurodegenerative disorder of the dopaminergic neurones in the substantia nigra. Parkinsonism is a clinical syndrome consisting of four cardinal features:  Bradykinesia (slowness and poverty of movement)  Muscular rigidity  Resting tremor (which usually abates during voluntary movement)  Impairment of postural balance leading to disturbances of gait and falling .
  • 4.  Most common neurologic disorder affecting approximately 1% of the population of individuals above 60years of age  7.5 million people world wide
  • 5.  The most common cause of parkinsonism is idiopathic PD, first described by James Parkinson in 1817 as paralysis agitans, or the "shaking palsy." The pathological hallmark of PD is a loss of the pigmented, dopaminergic neurons of the substantia nigra pars compacta, with the appearance of intracellular inclusions known as Lewy bodies.
  • 6.  Progressive loss of dopamine-containing neurons is a feature of normal aging; however, most people do not lose the 70% to 80% of dopaminergic neurons required to cause symptomatic PD.
  • 7.  Genetic factors(PARK2/7,PIN K1)  Environmental factors - manganese and pesticides  Drugs - antipsychotics (clozapine)  Cerebrovascular disease (stroke)  Smoking  Coffee
  • 8.  The primary deficit in PD is a loss of the neurons in the substantia nigra pars compacta that provide dopaminergic innervation to the striatum (caudate and putamen).since dopamine facilitates the inhibiton on a wide range of motor activities, release of this inhibiton causes in appropriate activation of these motor activities  The presence of lewy bodies
  • 9.
  • 10.  Stage 1 - Mild symptoms such as tremors  Stage 2 - Symptoms are bilateral  Stage 3 - Inability to walk straight or stand  Stage 4 - Rigidity and bradykinesia  Stage 5 - Unable to take care of themselves and requires a contant one on one nursing care
  • 11.  Cardinal Features -Resting tremors -Rigidity -Bradykinesia -Postural instability
  • 13.
  • 14.  Medical -Gene therapy -Dietary consideration -Deep brain stimulation -Neural transplantation -Speech therapy -Exercise and physical therapy -Pharmarcological therapy
  • 15.  Nursing -Assessment 1. •Do you have leg or arm stiffness? 2. •Have you experienced any irregular jerking of your arms or legs 3. • Have you ever been “frozen” or rooted to the spot and unable to move 4. • What specific activities do you have difficulty doing?
  • 16.  During this assessment, the nurse observes the patient for quality of speech, loss of facial expression, swallowing deficits,tremors  slowness of movement, weakness, forward posture, rigidity and evidence of mental confusion
  • 17.  Diagnosis 1. • Impaired physical mobility related to muscle rigidity and motor weakness 2. • Self-care deficits (feeding, dressing, hygiene, and toileting) related to tremor and motor disturbance 3. • Imbalanced nutrition, less than body requirements, related to tremor, slowness in eating, difficulty in chewing and swallowing 4. • Impaired verbal communication related to decreased speech volume, slowness of speech, inability to move facial muscles
  • 18.  Planning and goals  Improving functional mobility  Maintaining independence in activities of daily living  Achieving adequate bowel elimination, attaining and maintaining acceptable nutritional status  Achieving effective communication
  • 19.  Interventions Mobility - range-of-motion exercises promote joint flexibility - Warm baths and massage to relax muscles Self care - Teaching, supporting and encouraging the patient during activities of daily living promote self-care
  • 20. Nutrition - Monitoring weight on a weekly basis indicates whether caloric intake is adequate - Nasogastric tube maybe necessary as the disease progresses Communication - A speech therapist may be helpful in designing speech improvement exercises and assisting the family and health care personnel to develop and use a method of communication to meet the patient’s needs
  • 21.  Dopamine Agonists - levodopa combined with a peripheral decarboxlase inhibitor e.g cardidopa  Anticholinergics - benztropine mesylate for treatment of motor symptoms  MAO-Inhibitors - selegiline block the breakdown of dopamine
  • 22.  Acetylcholinesterase inhibitors (central) -Donepazil treatment of dimentia  COMT Inhibitors -Tolcapone inhibit COMT the major catecholamine degrader