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Pharmacology 2100 > Parkinsons > Flashcards

Parkinsons Flashcards

1
Q

what age does parkinsons usually show symptoms

A

60

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2
Q

signs of parkinsons

A 
rhythmic tremor-rolling a pill motion 
leaning forward and backward
muscle rigidity- jerky
difficulty rising from sitting 
shrinking of writing 
loss of spontaneous movements
bradykinesia- slow movement
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3
Q

how is movement controlled

A

signlas form motor cortex to spinal cord go to muscles

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4
Q

corticospinal tracts

A

from motor cortex to spinal cord

makes up the pyramids in the medulla

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5
Q

extra pyramidal system

A

basal ganglia signals to the cortex

controls movement without corticospinal nerves

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6
Q

voluntary motor pathways

A

upper and lower motoneurons
corticospinal pathway
piramidal tracts

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7
Q

involuntary motor pathways

A

extrapiramidal system
basal ganglia
reticular and vestibular system

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8
Q

what is parkinsons caused by

A

loss of neurons in substantia nigra and thus loss of dopamine innervation of striatum

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9
Q

when do symptoms appear

A

when 70% of nigrostriatal neurons are lost

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10
Q

what happens to gaba neurons normally

A

inhibited by dopamine and sitmulated by acetylcholine

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11
Q

what happens to gaba in parkinsons

A

dopaminergic neurons die so excess acetylcholine (stimulatory)

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12
Q

what happens to gaba in huntingtons

A

gaba and some acetylcholine neurons die

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13
Q

etiology of parkinsons

A

metabolism of dopamine by MAO B
environmental toxin
dopamine itslef an axidant
genetic pathway

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14
Q

what do COMT and DDC do

A

convert l-dopa before it can cross the BBB

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15
Q

di receptor dopamine subfamily

A

Gs adn increase camp

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16
Q

d2 dopamine subfamily

A

Gi and decrease camp

17
Q

striatum dopamine receptors

A

smooth muscle in periphery

18
Q

dopamine agonists

A

pramipexole

ropinirole

19
Q

first line therapy for parkinsons

A

levadopa

20
Q

how does l-dopa distribute in the body

A

rapidly absorbed from SI by amino acid transport system
crosses the BBB
peak concentraiton an hour after ingestion with 1-3 hour half life

21
Q

bioavailability issues with ldopa

A

metabolized in the intestine, blood, and periphery

only 1% actually enters the brain

22
Q

therapeautic effects of ldope

A

reduces rigidity and bradykinesia
improves motor function and speech
return of facial expression

23
Q

side effects of ldopa

A 
anorexia 
hypotension adn cardiac arrhythmias 
dyskinesias (involuntary movements) 
on-off effect becuase wears off
behavoiural changes 
insomnia confusion 
schizophrenia like behaviour
24
Q

why is carbidopa used in adjuncts with ldopa

A

inhibits dopa decarboxylase so less ldopa converted outside the BBB thus reducing the amount required and the adverse effects

25
Q

what does entacapone do

A

reversible inhibtors of peripheral COMT used in later stages
can enhance some adverse effects of ldopa such as dyskinesias

26
Q

what do ropinirole and pramipexole do

A

agonists of d2 and d3 receptors in and outside of corpus striatum that improves depressive symptoms

27
Q

side effects of dopamine agonists

A

action of d2 receptors outside of corpus striatum causes dyskinesia
activates other D receptors suppressing prolactin secretion, suppressing growth hormone release
hypotension
visual and auditory hallucinations

28
Q

examples of muscarinic antagonists

A

trihexyphenidyl

benzatropine mesylate

29
Q

who are the muscarinc antagonists used in

A

young patients wiht tremor to inhibit striatal cholinergic activity
not in the elderly

30
Q

muscarinic antagonist side effects

A 
dry mouth 
blurred vision 
urinary retention 
constipation 
mental confusion 
delusions 
drowsy
hallucination 
glaucoma
31
Q

what does MAO A do

A

metabolizes NE and serotonin

32
Q

what does MOA B do

A

metabolizes dopamine

33
Q

what does selegiline do

A

selectively inhibits MOAB to enhance ldopa effects and manage on off effect

34
Q

side effects of selegiline

A

insomnia
cognitive problems
dont use with MAOI

35
Q

why is rasagiline better than selegiline

A

less production of amphetamine like byproducts
better bioavailability
useful for depressed of poor cognitive function patients

36
Q

what does amantadine do

A

increase dopamine release in the CNS

37
Q

how is amantadine excreted

A

kidney takes 12-14hr

38
Q

side effects of amantadine

A

similar to ldopa

livedo reticularis-redblue netliek mottling of skin of the extremities with long term use due to vasoconstriction

39
Q

some non pharm therapies

A

surgery
deep brain stimulation
glial cell line derived neurotrophic factor
stem cells replace dopaminergic neurons

Pharmacology 2100 (13 decks)

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