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43 Cards in this Set

  • Front
  • Back
what are 3 proposed causes of Parkinson's disease?
1. age
2. genetics
3. environmental exposure
molecularly, inhibition of ___________ causes __________ aggregation, which causes death of the dopaminergic cell neuron.
mitochondrial complex I
How does CoQ10 fit into the parkison's picture?
CoQ10 stabilizes the mitochondria (it can block ATP depletion; therefore it blocks loss of striatal dopaminergic neurons)
genetic based models of PD propose mutations in which genes? (3)
1. Synuclein (encodes a-synuclein)
2. Parkin (known to cause recessively inherited PD)
3. Ubiquitin C-Terminal Hydrolase L1 (protein that recycles ubiquitin)
What protien is a major component of Lewy bodies?
when toxic insult occurs, what is the reaction of a-synuclein?
a-synuclein (if damaged by insult) could interfere with the ubiquitin proteasomal pathway -> a-synuclein aggregates and cannot be recycled by the proteosome.
which step is the rate limiting step in DA synthesis?
tyrosine hydroxylase (tyrosine -> levodopa)
What are the 3 main categories of differential diagnosis for PD?
1. Idiopathic Parkinsonism
2. Secondary Parkinsonism
3. Parkinsonism with other neuronal system degenerations
What could induce secondary Parkisonism? (4)
1. Drugs (antipsychotics, antiemetics)
2. Toxins (CO, Manganese, MPTP, Petrochemicals)
3. Strokes/lesions in substantia nigra projections
4. normal pressure hydrocephalus
In a Parkinsonian tremor, which muscle groups are most commonly involved? Does the tremor disappear during sleep?
distal muscles
resting tremor: present during rest, absent during sleep
What happens in the striatum when dopamine producing neurons die?
loss of DA release in the striatum causes an increase in Ach activity
name 8 drugs that can cause parkinsonism
Amitryptline (and other TCA's), Phenothiazines (Carbamezapine,Chlorpromazine, Chlorprothixene), Haloperidol, Meroclopramide, MPTP, Reserpine
normal people contain how much DA? What about a PD patient?
normal: 3-6 micrograms
PD - <0.1 microgram
In the striatum: DA is ________ whereas Ach is _________. (+) or (-)
DA is inhibitory
Ach is excitatory
A therapeutic drug for PD would have what action on Ach?
inhibition of Ach hyperactivity
High levels of Ach in the corpus striatum are responsible for what PD symptom?
rigidity (immobility)
What is the main MOA of levodopa?
increases the synthesis of DA
Why is tyrosine not used to increase DA levels? (2 reasons)
1. tyrosine hydroxylase is the rate limiting step: this step must be bypassed in order to raise the [DA].
2. tyrosine hydroxylase may be defective in PD.
When levodopa is administered, symptoms disappear in what order?
1. akinesia
2. rigidity
3. tremor
When levodopa therapy is stopped, symptoms re-appear in what order?
1. tremor
2. rigidity
3. akinesia
Oftentimes with levodopa therapy there is incomplete inhibition of the tremor and complete inhibition of the akinesia. Why is this?
levodopa has incomplete inhibition of Ach: this results in a tremor.
levodopa (by forming DA) completely eliminates akinesia.
What are the side effects of L-Dopa?
nausea without vomiting, development of involuntary movements, hypotension, tachycardia, on-off phenomenon
How would you reduce nausea using a carbidopa/levodopa medication?
You would increase the levels of carbidopa
What is the one thing you should never do when treating a PD pt. (that is on L-Dopa) with nausea?
NEVER use an anti-emetic (such as chlorpromazine, phenothiazine). They block the DA receptors.
When administering L-Dopa: what is peak dose dyskinesia?
at peak doses of medication pt develops choreic mvmts involving the hands, arms, legs and face.
Why should levodopa be used with caution on PD pts. with cardiovascular disorders?
DA stimulates beta-adrinergic receptors in the heart causing tachycardia. (DA is a catecholamine)
Chorea is caused by an excess in ___.
Chorea - DA
what is a possible explanation for the on-off phenomenon?
L-Dopa is converted to either DA or methyl dopa. methyl dopa is a false transmitter: it binds to DA receptors blocking them.
Why does levodopa/carbidopa reduce nausea when levodopa alone doesn't?
the CTZ lies outside the BBB, therefore when carbidopa lowers DA levels in the periphery there is less Da to stimulate the CTZ.
What is Selegiline? MOA?
neuroprotective agent
1. conserves DA (by (-) catabolism)
2. prevents formation of OH radicals
3. rescues dopaminergic neurons
What goes wrong in PD that causes formation of the OH radical?
activity of glutathione peroxidase is reduced in PD, therefore an excess of H2O2 builds up. This H2O2 gets converted to OH radicals.
What is bromocriptine?
DA receptor agonist
What is the MOA of amantadine?
blocks re-uptake of DA thereby increasing it's time in the synaptic cleft.
also, has an amphetamine like effect - causes the release of DA.
Which drug would you use to treat mild parkinsonism, drug induced parkinsonism or hemiparkinsonism? (amantadine or levodopa)
Which drug would you use to treat moderate to severe parkinsonism? (amantadine or levodopa)
Which PD drug class do you never prescribe to the elderly?
Acetylcholinergic drugs (trihexyphenadyl, benztropine)
What are 2 signs of impending toxicity with acetylcholinergic drug use?
urinary retention and tachycardia. must discontinue immediately
in fetal cell tranplantation used to treat PD, where are the cells transplanted to?
caudate or putamen
When neuroleptics block DA receptors, what symptoms could be observed?
1. lactation (tuberoinfundibular system)
2. parkinsonism (striatum)
3. antipsychotic effects
What neuroleptic has a low incidence of extrapyramidal side effects?
What are the five neuroleptic induced movement disorders?
1. akathisisa "motoric restlessness"
2. dystonia
3. parkinsonism
4. tardive dyskinesia (occurs when meds are removed)
5. neuroleptic malignane syndrome (most serious, potentially fatal)
Which drug commonly results in galactorrhea? MOA?
chlorpromazine. blocks DA receptors in ant. pituitary, this increases PRL production.
what drug do you give to treat galactorrhea?