Drugs For Movement Disorders

Front 1

Drugs used to Tx Parkinson's (11)

Back 1

Levodopa
Bromocriptine
Pramipexole
Carbidopa
Ropinirole
Diphenhydramine
Benztropine
Selegiline
Tolcapone
Entacapone
Amantadine

Front 2

Dopamine receptor agonists for Parkinson's (3)

Back 2

Bromocriptine
Pramipexole
Ropinirole

Front 3

Anticholinergics for Parkinson's (2)

Back 3

Diphenhydramine
Benztropine

Front 4

Decarboxylase inhibitor for Parkinson's

Back 4

Carbidopa

Front 5

Monoamine Oxydase Inhibitors (MAOI) for Parkinson's

Back 5

Selegiline

Front 6

COMT inhibitors for Parkinson's (2)

Back 6

Tolcapone
Entacapone

Front 7

Spasmolytic drugs for Huntington's (2)

Back 7

Baclofen
Dantrolene

Front 8

Antipsychotic drug for Tourette's

Back 8

Haloperidol

Front 9

Biochemical & neuroanatomical basis of Parkinson's

Back 9

d/o of the basal ganglia; characterized by tremor, rigidity, & bradykinesia

Front 10

Why is L-Dopa administered w/ a decarboxylase inhibitor?

Back 10

Carbidopa enhances the bioavailability of L-Dopa & reduces the S/E's caused by L-Dopa's peripheral conversion to Dopamine

Front 11

Biochemical & neuroanatomical basis of Parkinson's

Back 11

d/o of the basal ganglia; characterized by tremor, rigidity, & bradykinesia. There is a progressive loss of dopaminergic neurons that lead from the substantia nigra to the striatum, causing dopaminergic deficiency, leading to decreased excitation of the motor cortex

Front 12

Why is L-Dopa administered w/ a decarboxylase inhibitor?

Back 12

Carbidopa enhances the bioavailability of L-Dopa & reduces the S/E's caused by L-Dopa's peripheral conversion to Dopamine

Front 13

Properties of drugs that increase the bioavailability of L-Dopa & prolong the action of Dopamine

Back 13

L-Dopa is the most effective drug at Txing PD. L-Dopa is converted to DA both in the brain (where it effectively treats Sx of PD) & in the periphery where it 1. decreases the bioavailability of L-Dopa that can cross the BBB & Tx Sx of PD, 2. causes many A/E: N/V, psychosis & hallucinations, dyskinesias, dysrhythmias & orthostatic HOTN, fluctuations in therapeutic response
Dopamine receptor agonists do not require functional nigrostriatal dopaminergic neurons, they are less effective than L-Dopa, & have a higher incidence of psychotic S/E than L-Dopa; they act primarily on the Indirect pathway

Front 14

Dopamine's effect on Direct & Indirect pathways

Back 14

Activation of the Direct pathway disinhibits the thalamus, thereby activating the spinal cord motor neurons. Activation of the Indirect pathway increases the inhibition of the thalamus, thereby inhibiting the spinal cord motor pathway. Dopamine stimulates the motor pathway by increasing the Direct pathway & decreasing the Indirect pathway

Front 15

L-Dopa

Back 15

MoA: being a precursor of DA, it indirectly increases activity of spinal cord motor neurons
A/E: N/V, psychosis & hallucinations, dyskinesias, dysrythmias & orthostatic HOTN, fluctuation in therapeutic response, & compulsive behavior
End of dose deterioration: 1st manifestation of therapeutic fluctuation, occurs 2-3 hrs after a dose
Pearl: often administered w/ carbidopa

Front 16

Carbidopa

Back 16

MoA: enhances bioavailability of L-Dopa & reduces the S/E's of peripheral conversion of L-Dopa to DA by inhibiting peripheral decarboxylase

Front 17

Bromocriptine

Back 17

MoA:Ergot-derived D2 receptor agonist & D1 receptor antagonist
A/E: N, somnolence, postural HOTN, edema, hallucinations, confusion, & compulsive behaviors (more common than w/ L-Dopa)

Front 18

Pramipexole & Ropinirole

Back 18

MoA: Non-ergot-derived D2 agonist (no action @ D1)
A/E: N, somnolence, postural HOTN, edema, hallucinations, confusion, & compulsive behavior

Front 19

Benztropine & Diphenhydramine

Back 19

MoA: muscarinic antagonist
Ind: tremor & rigidity in PD
A/E: drowsiness, delusions, mood changes, dry mouth, blurred vision, exacerbation of memory loss & dementia
Pearls: little anti-PD effect & are usually used early in the dz

Front 20

Selegiine

Back 20

MoA: selective, irreversible inhibition of MAO-B (which is responsible for most oxidative metabolism of DA), thereby prolonging the action of DA, reduces effects of L-Dopa, end of dose & on-off phenomenon
Pearl: usually given w/ L-Dopa
Cont: tricyclics, SSRIs, or meperidine

Front 21

Tolcapone

Back 21

MoA: peripherally & centrally acting competitive inhibitor of COMT, thereby extending the bioavailability & duration of effectiveness of L-Dopa
Ind: pt's who don't respond to Entacapone
A/E: explosive diarrhea, hepatotoxixity (rare)

Front 22

Entacapone

Back 22

MoA: peripherally acting (only) competitive inhibitor of COMT, thereby extending the bioavailability & duration of effectiveness of L-Dopa

Front 23

Amantadine

Back 23

MoA: unclear; anti-viral
Pearl: only effective for 6-8 mo; usually given early in dz process

Front 24

Baclofen

Back 24

-muscle relaxer
MoA: GABA-B receptor (when activated result in hyperpolarization of neurons due to increased K+ conductance) agonist
Ind: MS, ALS, & traumatic spinal cord injury
S/E: weakness, drowsiness, & lowered SZ threshold

Front 25

Spasmolytic drugs are used to Tx?

Back 25

MS, ALS, Cerebral Palsy, & spinal cord injuries

Front 26

Dantrolene

Back 26

MoA: relaxes muscle by reducing Ca+ release from the sarcoplasmic reticulum
Ind: acute malignant hyperthermia-typically in children (triggered by general anesthesia, & neuroleptic malignant syndrome), cerebral palsy, & MS

Front 27

Haloperidol

Back 27

MoA: unknown
Ind: motor & vocal tics ass'd w/ Tourette's
A/E: multiple