TOXICOLOGY
COMPLICATIONS
■ Hypersensitivity reactionsmay occur 1–6 weeks after starting phenytoin
therapy, eg, SLE, TEN, erythema multiforme.
■ Gingival hyperplasiacan be seen with chronic phenytoin therapy.
■ Chronic ingestion of valproic acid: Hepatic failure
ANTIPARKINSONISM DRUGS
In Parkinson disease, cells in the substantia nigra degenerate, reducing the
production of dopamine, an essential neurotransmitter for the control of
movement and coordination.
The drugs used in the treatment of Parkinson disease can be divided into two
main groups: Dopamine agonists and anticholinergics (see Table 6.10).
Acute overdose of antiparkinsonism drugs is rare.
MECHANISM/TOXICITY
■ Dopamine agonists: Excessive activation of dopaminergic neurons. Activa-
tion of serotonergic systems may also occur.
■ Anticholinergics: Inhibition of central and peripheral muscarinic
receptors
■ Monoamine oxidase inhibition (selegiline): May become nonselective at
high doses →excessive circulating catecholamines.
SYMPTOMS/EXAM
Dopamine Agonism
■ Acute toxicity: Anxiety, confusion, agitation, insomnia, tachycardia,
hypotension
■ Chronic toxicity: Dystonia, hallucinations, hypersexuality, delusions
Anticholinergics
■ Anticholinergic toxidrome
TABLE 6.10. Drugs Used in the Treatment of Parkinson Disease
DRUG MECHANISM OFACTION
Dopamine Agonists
Levodopa Converts to dopamine
Catechol-O-methytransferase (COMT) Extend the duration of effect of levodopa
inhibitors
Selegiline Selective monoamine oxidase inhibitor, blocks
reuptake of dopamine
Bromocriptine Dopamine receptor agonist
Anticholintergics
Benztropine (and others) Inhibit the excess central muscarinic activity
caused by dopamine deficiency