Park+Crazies+Lithium

Front 1

what makes up the striatum

Back 1

caudate nucleus + putamen

Front 2

define parkinsonism

Back 2

degen. of dopaminergic neurons of the substantia nigra-so deficit of inhib. on cholinergic

Front 3

D1 path aka..
what does it do?

Back 3

direct pathway-stimulates motor activity

Front 4

D2 path aka

Back 4

indirect pathway-dopamine acting on this inhibits the indirect pathway(takes brake off)..think disinhibition

Front 5

maximal efficacy occurs when...

Back 5

both d1 and d2 are occupied by dopamine

Front 6

rate of neuron loss per decade

Back 6

3-15% per decade-we are in 3rd decade of life

Front 7

percent to be considered having parkinsons

Back 7

80% or >

Front 8

D1 like receptors

Back 8

D1 and D5

Front 9

D2 like

Back 9

D2,3,4

Front 10

Which receptor in striatum?
PFC?

Back 10

striatum-D1, D2
PFC-D1

Front 11

#1 excitatory neurotransm.
#1 inhinib?

Back 11

Glutamate-excit
GABA-inhib

Front 12

structures involved in finetuning

Back 12

Extrapyramidal NS.-Thalamus

Front 13

Niagra striatal pathway is involved in?

Back 13

movement

Front 14

Dopamine's effects

Back 14

D1-motion
D2-inhibits brake(motion)
Ach- inhibits brake

Front 15

R.L. step of dopamine synth.

Back 15

tyrosine hydrolase

Front 16

MAO-A where? and what?
MAO-B-where and what?

Back 16

A-in liver-NE, 5HT, DA
B-brain-DA

Front 17

how does L-dopa reach brain?

Back 17

actively transp. by LNAAT in epithelium and brain

Front 18

dopa decarboxylase requires what? and what does it do?

Back 18

requires coenzyme vit b-6
converts L-dopa to dopamine(can prematurely convert it in liver)

Front 19

COMT does what?

Back 19

can convert L-dopa to inactive metab. which competes for transporter

Front 20

what kind of changes in behavior for park?

Back 20

initiall change-sad to happy (low dope to high)

Front 21

L-dopa makes dopamine which inhibits?

Back 21

prolactin(hypoprolactemia) in A.Pituit.

Front 22

most effect. tx for park?

Back 22

L-dopa 50% incr.

Front 23

4 cardinal sytmptoms of park?

Back 23

-resting tremor
-pill rolling-first sign
-akinesa
-cogwheel rigidity

Front 24

mental ability of park patients? affect or not?

Back 24

not impaired

Front 25

parkinsons disease is a ______ disease

Back 25

idiopathic
but maybe due to toxins-MPTP, CO2 posioning, manganese

Front 26

carbidopa, what does it do and where?

Back 26

inhibits decarboxylation peripherally-can't cross BBB(good)

prevents premature conversion of L-DOPA

Front 27

MAO-A, B which one can be combined with dopa?

Back 27

B- if A is used you prevent breakdown of Dopamine--->NE so cause hypertensive crisis

Front 28

pt taking just dopa causes?

Back 28

N+V-from D2 in CTZ

Front 29

relief from dopa lasts for how long

Back 29

5 years

Front 30

how to tx wearing off or end dose akinesia?

Back 30

smaller dose or more frequent intervals or CR

Front 31

On-off phenomenon is

Back 31

NOT simply blood leveles

Front 32

Drug holiday for S.E.

Back 32

may help in dopa tx S.E. but little help for on-off phenom.

No longer reccom.

Front 33

Where is COMT found?

Back 33

gut, liver, brain

Front 34

benztropoine and trihexyphenidyl

Back 34

prototype anticholinergic drugs for parkinsons

all same efficacy-improve tremor

Front 35

Amandtadine

Back 35

mainly blocks NMDA
increases presynaptic dopamine, mild anticholinergic effects

can be mono, usually adjunct therapy
not metabolizes-kidney excretes
S.E.-purpleish skin
limited effectivness-6 to 9 months

Front 36

blocking NMDA benefits what?

Back 36

effect on ridgity + akinesia
anti-dyskinesic due to NMDA block

Front 37

Bromocriptine

Back 37

D2 receptor agonist, mild D1 antag
t1/2 is 4 x than Dopa

fewer long-term motor fluctuations
eventually benefits decrease

Front 38

S.E. of Bromoctriptine

Back 38

Orthost hypotension
syncope(fainting)
N+V-D2
hallucinations-reason ppl discontinue
pedal edema

Front 39

Pramipexole and ropinirole

Back 39

non-ergot dopaminergic agonist
-D2 and D3
approved for early and advanced pakinsons
-Same S.E. as bromocriptine
causes sudden sleep atacks-all dopamine agonists too

Front 40

Apomorphine

Back 40

non-ergot dopamine agonist
-tx of hypomobility(off episodes)

Front 41

S.E. of apomorphine

Back 41

N+V, must be taken with anti-emetic like Tigan

increased woody-Europe
contra-ondansetron + 5hts recp antag.
contains sulfites

Front 42

Rotigotine

Back 42

non ergot dopamine agonist, D2
also at D1, D3

first patch form, for parkinsons

Front 43

Adv. of DA agonists vs L-Dopa

Back 43

no comp with AA for LNAAT
no metab. for activation
incr reliability, potency(not efficacy)
dec. risk of dyskinesias
metab. does NOT prod free radicals

Front 44

Tolcapone and Entacapone

Back 44

revers. COMT inhibitors
prevent conversion of Levodopa to inactive 3-O-methyldopa, competes for transport

Front 45

3-O-methyldopa

Back 45

inactive levodopa, half-life is *15 hours*

Front 46

COMT inhib.

Back 46

Tolcapone-inhibit in CNS and Periph.
Entacapone-inhibit in periph.

used for adjunct therapy

Front 47

Tolcapone S.E. (think TACOS)

Back 47

explosive diarrhea
hepatotoxicity-discontinue use if levels >5

Front 48

Selegline

Back 48

formerly deprenyl
MAO-B inhib.
high does-loses specificity
monotherp.-only works for months
mainly adjunct

Front 49

Selegline S.E.

Back 49

metabolized into amphetamines-insomnia if does after 2pm

dyskinesia, confusion, psychosis

Front 50

Anti-oxidant drugs that counteract dopamine oxidation

Back 50

MAO-B inhib
Vit. E

Front 51

Oxid of dopamine via MAO leads to

Back 51

free radicals....H202-->OH*(free radical)

Front 52

Rasagline

Back 52

MAO-B inhib. (14x more selective for B)

5x more potent than selegiline
**NOT metab to amphetamine**
metabolized by CYP A12

Front 53

most eff Early tx of parkinsons
dopamine agonists vs levodopa

Back 53

dopamine <levodopa

Front 54

dopamine agonists are more likely to produce ________ and less likely to produce_________

Back 54

neuropsychiatric problems
dyskinesias

Front 55

define Tic

Back 55

repetitive motion
can be partially suppressed by voluntarily controlled

Front 56

define chorea

Back 56

rapid, flick-like movements of limbs-like restlessness

Front 57

athetosis

Back 57

slow, writing movements of extremities

Front 58

ballismus

Back 58

violent, flailing movements-proximal limbs

Front 59

postural tremor

Back 59

maximal when limb is in static motion-arms stretched out in bird wing
associated with hyperadrenergic states-from amphetamines, cocaine

gener. and abated by peripherie adrenergic
blocked by propanolol-B1 and B2!

Front 60

kinetic(intention) tremor

Back 60

maximal when in movement, NOT at rest