Drugs on Exam 3 Flashcards
Carbidopa
Parkinson’s
Dopamine Precursors / DDC inhibitors
Levodopa/Carbidopa
Parkinson’s
Dopamine Precursors / DDC inhibitors
Endogenous precursor to DA. Very short acting; peak action 30-60min, cleared in 2 hours
L-DOPA is an intermediate produce in the synthesis of dopamine endogenously. Since Parkinson’s is a disease of too little dopamine synthesis, giving L-DOPA can help replenish some of the missing dopamine in the brain. Carbidopa cannot cross the BBB but can inhibit degradation of L-DOPA in the guy and liver by blocking dopamine decarboxylase. Thus, by giving L-DOPA with carbidopa, you can deliver a high dose of L-DOPA to the brain where it can be converted to dopamine in the basal ganglia.
ADRs: Acute nausea, hypotension, depression, and psychosis
Chronic dyskinesia and psychosis
Anticholinergic Drugs
Parkinson’s
When there is loss of dopamine, there is over-activity of cholinergic interneurons in the putamen and caudate (DA inhibits ACh). The anticholingerics used in Parkinson’s block muscarinic receptors. These drugs are less effective than L-DOPA, but are sometimes used as initial therapy for tremor. However, side effects make these drugs difficult to tolerate.
Monoamine Oxidase Inhibitors
Parkinson’s
MAO is responsible for breaking down dopamine into DOPAC. By inhibiting this action, the effects of dopamine (and L-DOPA) can be potentiated. There are two types of MAO A and B. MAO-A has dangerous side effects because it affects the breakdown of many different monoamines (EPI, NE, 5HT, DA), limiting therapeutic use to MAO-B inhibitors, which are dopamine specific
Catechol-O-Methyltransferase Inhibitors
Parkinson’s
COMT is also part of the metabolism pathway of L-DOPA and dopamine. Giving COMT inhibitors can potentiate the effects of these molecules, making L-DOPA dosing less frequent.
Prostaglandin analogs
Glaucoma
ie Latanoprost
- Lower IOP by facilitating aqueous humor outflow through accessory uveosclero pathway
- First-line therapy in open-angle glaucoma as part of stepped approach
- Side effects include brown discoloration of iris, eyelash lengthening, and ocular irritation
Alpha-2 adrenergic agonists
Glaucoma
ie. Brimonidine
- Increases uveoscleral outflow pathway and inhibits aqueous humor production
- Add-on 2nd or 3rd line therapy in open-angle glaucoma
- Side effects include red eye, ocular irritation, CNS depression and apnea in neonates
Beta-adrenergic antagonists
Glaucoma
ie Timolol
- Reduces aqueous humor production
- Next most common drug used for open-angle glaucoma after prostaglandin analog
- Side effects include systemic absorption leads to decreased HR, bronchoconstriction, etc
- CONTRAINDICATED in Pts with bradycardia, heart block, CHF, asthma and COPD
Carbonic anhydrase inhibitors
Glaucoma
ie Dorzolamide
- Inhibiting CA in ciliary body epithelium reduces bicarb ion formation, leading to reduced fluid transport and IOP
- Add-on 2nd or 3rd line in open-angle glaucoma
- Side effects are few if applied topically
Cholinergic Receptor Agonists
Glaucoma
ie Pilocarpine
- Lowers IOP through contraction of ciliary muscle (increases aqueous outflow)
- Used in treatment of closed-angle glaucoma
- Not commonly used today for open-angle glaucoma
- Side effects include Ciliary spasm leading to HA, myopia, dim vision
tetrabenazine
Tourette syndrome and Huntington’s disease
Dopamine depleting drug
neuroleptics-aka dopamine receptor antagonist
Tourette syndrome and Huntington’s disease
Fluphenazine, aripiprazole
Side effects: weight gain, sedation
primidone
Essential tremor
propranolol
Essential tremor
Ropinirole
Parkinson’s
Dopamine Receptor Agonist
D2 receptor agonist (also D3 and D4)
ADRs: Nausea, Changes in mentation, Sudden onset of sleep
