Pharm Test 2- Parkinson's And Movement Disorders

Front 1

T or F: Parkinson's is due to genetics only

Back 1

F (genetic predisposition and exposure to an environmental stressor)

Front 2

Parkinson's disease symptoms are caused by what?

Back 2

a loss of dopaminergic neurons in one structure within the basal ganglia: the substantia nigra pars compacta (SNpc)

Front 3

It is thought that ___ ____ formations within dopaminergic neurons cause cell death in Parkinson's

Back 3

Lewy bodies

Front 4

T or F: only 25% of neurons in the SNpc need to be gone before Parkinson's develops

Back 4

F...85%!

Front 5

In parkinson's the ____ pathway sends an inhibitory signal to the ____. This pathway facilitates/inhibits movement and activity here is increased/decreased in parkinson's. Why is activity altered like this in Parkinson's?

Back 5

Indirect; thalamus; inhibits; increased (decreased acitivty of the direct pathway); the SNpc's dopaminergic neurons have died

Front 6

Dopamine can/cannot cross the BBB. L-dopa, the dopamine precursor, is/isn't actively transported across the BBB.

Back 6

cannot; is

Front 7

Why is L-dopa given with a decarboxylase inhibitor?

Back 7

because dopa decarboxylase converts L-dopa to dopamine PERIPHERALLY, thus less L-dopa gets to cross the BBB (dopamine cannot cross BBB).

Front 8

What is Carbidopa? Does it cross the BBB?

Back 8

a peripheral decarboxylase inhibitor; no

Front 9

What is Sinemet or Atamet? How is it dosed?

Back 9

Carbidopa:L-dopa 25:100 or 25:250; TID or 5x/day

Front 10

It is important to take Sinemet/Atamet on a full/empty stomach.

Back 10

EMPTY (competes with LNAA transporter; if nausea develops, you may have pt eat b4, but be aware that dose must increase)

Front 11

T or F: Dyskinesias are COMMON in pts taking Sinemet/Atamet long-term.

Back 11

T...80% of these pts

Front 12

Explain what On/Off means in relation to therapy with L-dopa.

Back 12

As the disease progresses, the ability for dopaminergic neurons to store dopamine is diminished and a period of akinesia (off) develops at the end of the pts regular dose...increased doses with shortened periods initially help. The decreased "buffering" causes ON symptoms as well, resulting in uncontrolled movement (dyskinesia...probably from too much drug?)

Front 13

When fluctuations in L-DOPA response occur (On/Off), what can be given when "off" periods are severe?

Back 13

SubQ Apomorphine (can provide temporary relief)

Front 14

________ is contraindicated in those with psychoses, angle closure glaucoma, and also in those taking MAO inhibitors.

Back 14

Sinemet

Front 15

Abrupt withdrawal of L-dopa can lead to what?

Back 15

Neuroleptic malignant syndrome

Front 16

What class of drugs are not dependent on enzymatic conversion to dopamine, have longer effectiveness than L-dopa, and have reduced fluctuations?

Back 16

dopamine receptor agonists

Front 17

Which is more beneficial when giving dopamine receptor agonists: D1 or D2 activation?

Back 17

D2 activation (inhibits the inhibitory pathway aka indirect pathway)

Front 18

Which of these agents have mixed activity? Which are D2 specific?
1. bromocriptine
2. ropinirole
3. pramipexole
4. pergolide
5. apomorphine

Back 18

1 and 2= D2 specific
3-5= mixed D1 and D2 activity

Front 19

Which dopamine receptor agonist is a partial agonist to the D2 receptor and antagonist to the D1 receptor?

Back 19

Bromocriptine

Front 20

Which dopamine receptor agonist requires co-admin of an anti-emetic (Domperidone)?

Back 20

Apomorphine

Front 21

T or F: dopamine receptor agonists can cause cardiac arrhythmias (alerting you to discontinue the med)

Back 21

T

Front 22

T or F: there is a thought out there that L-dopa may contribute to oxidative stress and kill more neurons

Back 22

T

Front 23

What is the "cheese effect"? What has been developed to alleviate it?

Back 23

When ingested orally, MAOIs inhibit the catabolism of dietary amines. When foods containing tyramine are consumed (so-called "cheese effect"), the individual may suffer from hypertensive crisis; MAO-B specific inhibitors relieve this

Front 24

What are the MAO-B specific inhibitors? What are they combined with during treatment?

Back 24

Selegiline, Rasagiline; combined with L-DOPA (Sinemet/Atamet)

Front 25

T or F: Selegiline and Rasagiline are reversible.

Back 25

F!

Front 26

TQ: What drug (and drug class) do you need to know about when prescribing Selegiline/Rasageline? What does mixing these cause?

Back 26

Meperidine (tricyclic SSRIs); serotonin syndrome

Front 27

What two drugs are inhibitors of COMT? Which one is only for peripheral actions?

Back 27

Tolcapone and Entacapone; Entacapone

Front 28

What side effect of Tolcapone have cause deaths?

Back 28

Liver failure...need liver function monitoring in pts taking this

Front 29

Benztropine, Trihexyphenidyl, and Biperiden are all what? When are they useful in the disease process?

Back 29

Antimuscarinics; early (used initially with predominant tremor...don't work so well with bradykinesia)

Front 30

What anti-Parkinson's drug is also used as an antiviral for Influenza A? When is it used in the diesease process?

Back 30

Amantadine; (initially with predominant tremor)

Front 31

T or F: if the pt exercises early on, Parkinson's has a chance of not fully developing and L-dopa therapy won't be necessary

Back 31

F!!! all will need L-dopa eventually

Front 32

What drugs are needed for Parkinson's early--->late stage

Back 32

Initial therapy: Selegiline
Initially with predom. tremor: Antimuscarinics or Amantadine
Increasing disability: dopamine replacement therapy: Sinemet and/or dopamine agonists
With progression and fluctuations: L-dopa plus either COMT or MAO inhibitors