Parkinson's Disease Flashcards

1
Q

Differentiate between Parkinsonism and Parkinson’s Disease

A

Parkinsonism
- a neurologic syndrome or group of symptoms, spcifically motor symptoms
- can be atypical parkinsonsim (lewey body, supranuclear, corticobasal), drug-induced or vascular as the cause

Parkinson’s Disease
- a neurodegenerative disorder of the CNS as a result of idiopathic loss of dopamenergic neruons
- also can be called idopathic parkinsonism
- genetic in nature or idopathic

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2
Q

so what is Parkinson’s Disease by Definition

predispositions?

A
  • a neruodegerative disorder that can be seen as a “shaking palsy”
  • idopathic in nature but there are some environmental and genetic predispositions
  • AGE IS THE MOST POTENT RISK FACTOR FOR PD: 2nd most common age related neurodegenerative disorder
  • risk doubles each decade after 50

Predispositions
- Genetics: GBA & LRRK2 & others
- Environment: pesticide use, rural areas, well water, and MPTP neurotoxin use (can be seen in street drugs
- can come on after a physcial trauma: like a fall or broken arm

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3
Q

Etiology of PD

normal role of dopamine in the body

A

a disease of the basal ganglia

BG strucutres
- caudate
- putamen
- nucleus accumbens (reward pathway)
- GP interna and externa
- subthalmatic nucl.
- substantia nigra these is where we see the dopamine depleteion

Dopamine: what does it do
- a monoamine neurotransmitter
- functions in : movement, memory, behavior, attention and cognition, sleep, arousal and mood
- naturally: its broken down my MAO, COMT, ALDH

specifically motor function: relies on the dopamine to project from the substantia nigra to teh dorsal struatum: when this is lost we see the results/symptoms of PD

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4
Q

Pathophysiology of PD

A

a decreased level of dopamine
- there is cellular death in teh substantia nigra
- the lackof dopamine in the SN leads to motor dysfunction

pathologically see: Lewy bodies on autopsy
- these lewy bodies are intracellular inclusions (aka protein buildups) of the alpha synuclein protein that gets built up and forms these lewy bodies, less dopamine produced and decrease motorfunction

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5
Q

Symptoms and cardinal features of parkinson’s disease

A

Cardinal Symptoms of PD: motor dysfunctions

  • Bradykinesia: slowed movements this is NEEDED to make the diagnosis of parkinson’s disease
  • Resting Tremor
  • Muscular Rigidity: cogwheel or leadpipe rigitiy on passive ROM
  • Postural instability: not caused by other visual, vestibular, cerebellar or proprioceptive dysfunction
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6
Q

Explain the details of Bradykinesia
how to test your pateints

A

Brady = slow kinesia = movements
because the lack of dopamine is a gradual progression/loss - the progression of symptoms will also be gradual

  • lack of spontaneous movements
  • loss of iADLS and ADLS
  • freezing of gait & movements

Ways to Test for Bradykinesia
- UE: finger tapping, hand opening, pronation&supanation
- LE: toe tapping and heel stomping

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7
Q

Tremor of PD patients
- characteristics of it
- how to test

A

Tremor of PD
- a resting tremor; described as “pill rolling” sititng with hands up
- can be bilateral, but most pt. have one side worse than the other
- frequency of the tremor: 3-5 Hz frequency

most pts. will have the tremor at the time of diagnosis

Tremor Characteristics
- accentuated by mental concetration: when you tell them to focsu on something in their head, it will come out
- upon postural changes; it may go away but will reappear (differ from procedural tremor)

How to test
- notice it during exam
- have pt. put arms out front and hold still
- make them thing about something (mental concentration)
- see the tremor reappear

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8
Q

Rigidity of PD pts.
how to test

A

Rigidity
- of the neck, shoulders, wrists and legs

Signs
- shown by decreased ROM
- decreased arm’s swinging during gait
- Cogwheel with passive ROM testing: ratchet-like jerks on exam when trying to passive ROM them

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9
Q

Postural Instability of PD pts.
how to test

A

Postural Instability

presents
- inability to be balanced when standing
- difficult ot make turns; take many little steps tp turn
- can increase fall risk

Test
- Retropulsion Test: stand behind them and pull their trunk backwards, they should take 1-2 steps to stabilize themselves; but a complete loss of balance = postive test
- or can tell their instability of gait upon exam seeing them enter the room

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10
Q

Specific aspects of your Pts. gait that may make you think they have PD

A
  • decreased arm swing
  • shuffling gati
  • stopped posture
  • freezing of gait (doorways and upon turning)
  • reemergence of tremor
  • en-block turning (little baby steps)
  • festation: during walking their steps are small and shuffle-like
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11
Q

Secondary Symptoms of PD

A
  • hyposomia
  • REM behavior disorder: reported by bed partner that they’re acting out their dreams
  • constipation: because they’re moving less
  • hypophonia: soft speech
  • micrographia: small handwriting
  • mypomimia: loss of facial expression “marked facies”
  • increase saliva
  • mood changes
  • cognitive impariment
  • fatigue
  • dysphagis (becuase of muscles)
  • difficulty with dexterity and turning in bed
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12
Q

Diagnosis of PD

A

the diagnosis of PD can be made clinically, with the cardianl symptoms present
- first; you need to rule out parkinsonism as a result of other etiologies (like drug-induced)
- a trial of Levodopa with efficacy can help

DAT scan to confirm the diagosis (dopamine transporter scan - DA SPECT)
- a NEGATIVE scan does NOT rule out the diagnosis
- not necessary to do but can be definitive in diagnosis
- results: “comma shape” = normal a “period shape” indicates a lack of DA in the brain

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13
Q

how to differentitae between PD and an essential tremor

A

Parkinson’s Disease
- a RESTING tremor
- can be bilateral; but one side will be worse than the other

Essential Tremor
- action tremr: present when they are moving
- present in the arms, the head and the voice
- the ET will improve with alcohol use

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14
Q

Nonpharmacologic Treatment of PD

A

Exercise!: the only way to SLOW progression of the disease is through exercise
- 30 minutes at least 4x/week
- variety in exercise will produce best results

Physiacal Therapy
- ambulation & balance training
- freezing of the gait
- abulation device for safer moving

Occupational Thearpy
- gait, bathroom saftey and device use

Speech Therapy
- to increase voice; loud therapy
- cognitive therapy

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15
Q

When do you start medication in your PD pts?
what med do you start first

A

medication are used to help with the symptoms of the disease; they are not able to curve or even stop neruoprogression
when to start? use the pt. ability and level of functioning to gage when medications should be introduced

FIRST LINE MEDICATION: Levodopa: a dopamine replacement medication (the precursor to dopamine)

Second-line: Dopamine agonists: but these can cause non-motor side effects (avoid in pts. > 70)

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16
Q

Levodopa/Carbidopa
- how does it work
- what does the addition of carbidopa do
- how to dose (generally)

A

Levodopa: a dopamine precursor: converted to DA once in the CNS and in the periphery

Carbidopa: an add on within the formulation; help to reduce the peripheral conversion of DA (becuase you really only need to DA to be converted within the CNS)
- also helps to decrease the N/V and GI side effects that levodopa has
- does not cross the BBB

Dosing
- strat very slow, with like 1/2 tablet and slowly increase to 1 tablet 3x daily
- titrat up for optimal symptom control

17
Q

Side Effects of CD/LD

Motor Complications: Response Duration

A
  • nausea/abd. cramping : this is where the addition of more carbidopa can be helpful to decrease these effects
  • Dyskinenas: wiggling movements as a result of too much DA in the body (at peak or during wear off)
  • Orthostatic Hypotention
  • Hallucinations (visutal or auditory)
  • “On-Off” phenomenon (fluctuation in thier motor symptoms; which is why its dosed multiple times a day
  • Dystonia: foot or cervical; abnormal posturing

Motor Complications with CD/LD
- the levodopa response duration shortens with increase use of the medication & with teh progression of the PD
- with progression of parkinson’s disease: the therapeudic window of levodopa shortens, making it harder to achieve motor symptom control without getting additional dyskinesia SE along with the medication
- a pulsitile stimulation of declining number of receptors lead to hypersensitivity of the receptor to the medication

18
Q

ways in which medication dosing can help try to combat the motor complications and decrease effectiveness of CD/LP with progressive PD

A

Immediate release and controlled release formulations exists
- controlled release: good for those who need it overnight to wake up without crazy intesne symptoms

a combo: of IR/CR = help to improve ON time without dyskinesia & motor function

  • enteral levodopa and oral inhalation exist
19
Q

Dopamine Agonists: second line medication for PD

A

Dopamine Agonists: directly increase the amount of dopamine wihtin the body

Ropinirole
Pramipexole

when to start
- can be introduced when levodopa response is variable
- starting thease earlier in younger pts. : can help delay the need to start levodopa as soon

these have less nausea and GI side effects

SE
- IMPLUSE CONTROL DISORDER: gambling, risky behavior: failure to resistn tempation or urge (hypersexual, eating, gambling, etc.) because DA is in teh reward pathway = reduce or d/c med, councel and education via CBT
- sudden sleep attacks
- othrostatic dizzy

20
Q

MAO-B INhibitors for PD
when to use

A

MOA-B Inhibitors: MAO breaks down DA: so if you inhibit their ability to breakdown –> you get increase DA in the body

Selegiline & Rasagiline
- well-tolerated, improve ON time, possible neuroprtective

SIDE EFFECTS = are huge and not great
- lots of D-D interactions: tyramines, SSRI/SNRI, meperidine, dextamethorophan
- possibly exacerbates dyskinesia and orthostatic hypotensions

21
Q

COMT INhibitors for PD
- what are they
- how do they work
- side effects

A

COMT INhibitors
Entacapone : inhibits peripheral conversion of levodopa: therefore helps with ON time of levodopa activity
must be taken with levodopa, its only role is to help the action of levodopa

Side Effects
- diarrhea
- orange urine
- dysnkinesia
- hallucinations
- low BP

22
Q

Amantadine for PD
how does it work
side effects

A

Amatadine; glutamte antagonist
- non-competitive antagonist of NMDA glutamatergic receptors –> thought to help increase levels of DA in the brain (dopamenergic)

Side EffeectS: mild anticholenergic effects
- dry mouth, urinary retention
- constipation
- hallucinations
- livdeo reticularis

mainly used to add on to levodopa and help reduce the dyskineasia assocaited with it
- also seen to help the tremor

23
Q

how to combat the confusion and psychosis of PD

A

always attempt to simplfy the medications & use the most effective and lowest dose possible of dopamenergic agents

to combat the halucinations
- Nuplazid

to combat the psychosis (use anti-psychotics with the lease extrapyramidial side effects)
- quetiapine
- cloazapine

24
Q

The role of Deep Brain Stimulation in PD

A

DBS
- microelectrodes implanted into the Basal ganglia: eithe rhte STN or the GPinternus to help with PD symptoms
- an implantable pulse generator is there to stimulate via high frequency
- its adjustable and reversible - safe once implanted

Indications
- those with refractory symptoms or medication side effects
- those who respond well to medication (but maybe cant tolerater SE) are best canidates with best outcomes of DBS
- contraindicated in those with PD dementia

need to have
- neurology
- nerurosurgery and neuropsychology invovled to plan & get full evlauation of pt. on and off medications and see levodopa effects first

25
Q

Atypical Parkinsonism

A

Lewy Body Dementia
- early onset dementia
- hallucinations
- cognitive fluctuations are a key: very drastic changes

Corticobasal Degeneration
- loss of sensation
- alien limn phenomenon

Progressive Supranuclear Palsy
- gaze palsy
- early cognitive and gait impairments
- speech impairments

multisystem atrophy
- autonomic insuffiency
- incontinence
- cerebellar ataxia

all of these atypical parkinsonsim’s will not respond well to the use of levodopa

26
Q

what type of medications will cause drug induced parkinsonism

A

Dopamine Receptor Blockers
- things which deplete dopamine thus mimicking PD

Typical Antipsychotics
- haldolol, phenothiazine, pimozide

Atypical Antipsychotics
- risperidone, olanzapine, ariprazole, ziprasidone

Dopamine Depleteing Agents
- Reserpine, tetrabenzine

Anti-Emitics
- Metoclopramide!!!