Disease specific drug

Question 1

Parkinson: dopamine agonist

Answer 1

Dopamine agonist: bromocriptin (ergot), pramipexole, ropinirole (non-ergot), non ergots are prefered

Question 2

Parkinson: increase dopamine

Answer 2

Amantadine: may increase dopamine release, also used in influenza A and rubella, toxicity=ataxia

L-dopa/carbidopa: converted to dopamin in CNS

Question 3

Parkinson: prevents dopamine breakdown

Answer 3

Selegiline (MAO type B inhibitor) vs.
(MAO breaks down everything)

COMT inhibitor (only dopamine breakdown): prevent L dopa degradation
- entacapone(central), tolcapone (central and peripheral)

Question 4

Parkinson: curve excess cholinergic activity

Answer 4

Benztropine (antimuscarinic: improves tremor and rigidity but has little effect on bradykinesia)

Question 5

Parkinson treatment

Answer 5

Loss of dopaminergic neurons and excess cholinergic

BALSA:
Bromocriptin
Amantadine
Levodopa (with carbidopa)
Selegiline (and COMT inhibitor)
Antimuscarinic

For essential or familial tremors, use beta blockers.

Question 6

L-dopa (levodopa)/carbidopa

Answer 6

MOA: increases dopamine in brain, unlike dopamine, L-dopa can cross blood brain barrier and is converted by dopa carboxylase in the CNS to dopamine

Carbidopa is peripheral decarboxylase inhibitor, is given with L dopa to increase the availability of L dopa inthe brain and to limit peripheral side effects

Clinical use: parkinson

Toxicity: arrythmias from increased formation of catecholamines. Long term can lead to dyskinesia following administration, akinesia between doses.

Question 7

Selegilin

Answer 7

MOA: Selectively inhibit MAO-B, which preferentially metabolizes dopamine over NE or 5-HT, thereby increasing the availability of dopamine

Clinical: adjunctive agent to L dopa in treatment of Parkinson
Toxicity: may enhance adverse effect of L dopa

Question 8

Alzheimer’s drug

Answer 8

Memantin:
MOA: NMDA receptor antagonist, helps prevent excitoxicity (mediated by Ca2+)
Toxicity: dizziness, confusion, hallucination

Donepezil, galantamine, rivastigmine
Mechanism: cholineserase inhibitor
Toxicity: nausea, dizziness, insomnia

Question 9

Huntington’s drug

Answer 9

NTM changes: low GABA, low ACh, high dopamine

Treatment:
Tetrabenazine and reserpine: inhibit VMAT; limit dopamine vesicle packaging and release

Haloperidol: dopamine receptor antagonist

Question 10

Sumatriptan

Answer 10

MOA: 5HT 1B/1D agonist
Inhibit trigemnial nerve activation, prevents vasoactive peptide release; induce vasoconstriction. Half life s angina), mild tingling