Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

62 Cards in this Set

  • Front
  • Back
PD epidemiology
1.5million people in US
85% over 65

familial(genetic) PD in 10% of cases
4 Cardinal Symptoms of PD
1. bradykinesia- slow mvmt
2. Muscle Rigidity- veloc indep
3. Tremor- classic, at rest
4. Gait Instability
PD Tremor
primarily at REST
goes away w/ purposeful mvmt
often starts in thumb at 4Hz
Stage 1

Stage 2

Stage 3
1. classic presentation, asymmetrically
2. spreads bilat, postural changes,gait changes
3. pronounced gait problems, unstable
Stage 4

Stage 5
4. further progression, needs assistance walking
5. wheelchair, bed-ridden. Eng Stage of PD
Unified PD Rating Scale
scaled from 0-199 (total disability)
Non-Cardinal Symptoms
ANS- sweating, drooling, dsyphagia, seborrhea, constipation
what type of diagnosis is PD?
clinical diagnosis, from the symptoms alone
Lewy Bodies
bottom of the dopamine producing cell of the SN
light pink w/ pink halo\

*Have a PROTECTIVE effect- buy time
what form prior to Lewy Bodies?
Pale bodies
these are the cells that are more prone to die
Dopamine projection into striatum via...
Direct and Indirect pathways
both are hit in PD
how is PD a hypokinetic movement disorder?
GPi produces too much GABA
which symptoms improve with Dopamine treatment?
1. bradykinesia
2. tremor
3. rigidity
will dopamine help constipation?

depression in PD

b/c PD is a Monoaminergic deficiency disease
symptoms that are not responsive to medication...
1. postural instability(cardinal symptom)
2. freezing phenomenon
3. speech abnormalities
4. ANS symptoms
5. eye movements- progressive supranuclear palsy
6. dementia (15-20%)
dopamine receptors
5 total
2 in straitum: D1 and D2
D1-excitory- inc cAMP
D2-inhibitory- dec cAMP
Gold Standard for PD medications
precursor to dopamine and other catecholamines (epi, Norepi)
Problems w/ Levodopa
1. extrauncontrolled mvmts
2. has a short half-life
3. therapeutic window narrows w/ progression
on-off phenomenon
before patients get dyskinesia they dvlp these motor fluctuations
happens later in progression, levodopa doesnt work as long

carbidopa blocks periph production of dopamine
levodopa + carbidopa + entacapone
entacapone inc half-life
what is a major sideeffect of levodopa?
levodopa converted to dopamine in periphery stimulates the vomiting center
what is the gold standard medication in the US?
Sinemet: levodopa + carbidopa
dopamine agonists

dont have to be converted, cross BBB w/ ease
bind to dopamine receptor

3x's per day
a dopamine/rec stim patch
what two areas are degenerated in PD
1. SN
2. Locus ceruleus in pons
depression in PD due to
dec amounts of NE, dopamine, and Serotonin
what is the difference b/w idiopathic depression and PD depression?
somatic symptoms are much greater in PD depression
suicide not as great in PD depression

both have dec NE and Serotonin- treat w/ prozac
Sleep problems in PD
monoamines control sleep
98% of PD pts have sleep problems

use SSRIs if sleep too much
use Tricyclics if not enough
what is a sleep disorder that is predicative of PD?
REM sleep behavior disorder (RBD)

Klonopin is only med that helps RBD
do most patients w/ PD dementia have alzheimer's?
Lewy bodies in regular PD pts

Lewy boeies in PD w/ dementia
only seen in LC and SN neurons

also seen in cerebral cortex
called Diffuse Lewy Body Disease
cholinesterase inhibitor works better on which patients?
Alz or PD
PD w/ dementia
when PD patients have hallucinations what do you do?
1. cut DA agonists first
2. Cut Levodopa
Poorly Responsive PD variants
1. diffuse lewy body disease
2. progressive supranuc palsy
cant move eyes
3. corticobasal gangl degen
4. vascular parkinsonism
lacunar disease in BG
Drugs DO NOT work
what is a tremor indicative of?
NORMAL PD, treatable

no tremor means variant
Essential Tremor
type of PD variant
NOT a tremor at rest
tremor occurs when try to pick up something
familial, NOT responsive to dopamine meds
Multiple System Atrophy
PD variant. combination of OPCA, SDS, and SND
opca- very ataxic
Shy Drager syn- ANS, faints a lot
Striatonigral degen- doesnt respond to meds. axon terminal degen
Wilson's Disease
runs in PD families. mimics PD
lack of ceruloplasin protein that carries copper

Kayser-Flelscher rings around iris
Progressive Supranuclear Palsy
midbrain almost gone
problems moving eyes
Humming bird sign on CT/MRI
OPCA- olivopontinocerebellar atrophy
very clumsy and ataxic
Multiple System Atrophy

Striatonigral degen
get protein collections in oligodendrocytes (glia)

starts in putamen, end of the nerve endings are the problem
if the Putamen is damaged, what is the response to drugs?
this is where dopamine binds
D1 and D2
Corticobasal ganglionic degen
1. dont have a tremor
2. have apraxia- lose motor memory
3. Alien limb
Parkinsonisms where meds do not work:
1. Striatonigal degen
2. vascular parkinsonism
how many dopamine cells do you have to lose before getting symptoms?
environmental factors of PD
1. rural living
2. well water
3. industry of paper mill, iron smelting
The Movie Awakenings
showed cases of viral encephalitis that caused severe PD
2 Major Themes in PD
1. protein problems- aggregates
2. mitochondria poisoning
1st discovered cause of Familial PD
ALpha Synuclein Mutation
1bp change in gene
tons of lewey bodies result
Actinomyces bacteria
make proteosome inhibitors

may cause proteosome dysfxn
Oxidative stress

results in free radical generation
mpp poisons mitochondria
destorys catecholamine cells
dopamine broken down by..

GSH in PD brains....
by MAOB into chems, including H202
glutathione normally removes the peroxide
glutathione is absent in PD brains
Fenton reaction
w/o GSH, iron reacts w/ hydrogen peroxide to produce hydroxyl free radicals

free radicals break down the cell. rel Ca and turn on degredative NZMs
1st focus in treatment for PD
was on inhibiting MAOB nzm

it is of symptomatic benifit NOT neuroprotective
Rasagiline ($8/pill)
CoEnzyme Q10

Creatine and Minocycline
in ETC of mitochondria
some benifit, but need HUGE doses (1200mg qd)

may be neuroprotective

for PD

for Tremor
Deep brain stim
dystonia + PD(better)
adrenal cortex tissue transplants

using dopamine cells from retina
do not work

STEPS program, in clinical trials right now
what does the Fluora-Dopa Scan reveal?
L-dopa accumulates in Striatum
what is a problem w/ L-Dopa and disease progression?
the threshold for dyskinesia decreases as the disease progresses.
patients get dyskinesia (unable to control voluntary mvmts-wiggles)
Imaging is useful in distinguishing PD varients. especially....
2. CBGD-corticobasal ganglionic degeneration
2 theories on cause of PD
1. MPP+ kills mitochondria in catecholamine prod cells
2. Dopamine is conv to h202 and there is an absense of GSH, which allows the Fenton rxn
MAOB does 2 things
1. converts MPTP-->MPP+
2. Dopamine--> H202 and other side products