Læknaneminn - 01.10.1996, Page 91

Overdoses and poisonings: physiological responses
• Mediate a variety of cardiac eífects including an
increase in heart rate, conduction velocity,
contractility, automaticity, and rate of idiopathic
pacemakers.
fi -2 receptors:
• Mediate diverse effects which include smooth mus-
cle dilatation, insulin release, lipolysis, renin relea-
se, and gluconeogenesis. Clinically, these effects are
manifested as miosis, vasodilatation, broncho-
dilatation, hyperglycemia, decreased bowel motili-
ty, and bladder relaxation.
B. The Parasympathetic (Craniosacral)
Division
Acetylcholine is the neurotransmitter of the para-
sympathetic nervous system. Two types of cholinergic
receptors exist and are named muscarinic and nicotin-
ic.
1. Muscarinic receptors
These receptors are found in postganglionic para-
sympathetic fibers, autonomic ganglia, cortical and
subcortical neurons. Clinically, muscarinic effects
include:
• Miosis (constricted pupils)
• Vasodilatation (decreased blood pressure)
• Increase in bronchial secretions
• Decrease in heart rate, cardiac contractility, and
conduction
• Increase in bowel motility, micturation and sweat-
ing
Atropine competitively antagonises muscarinic
transmission.
2. Nicotinic receptors
These exist at autonomic ganglia and neuromuscular
junctions. Their sdmuladon results in:
• Initial contraction of striated muscles and fascicula-
tions followed by blockade of transmission manife-
sted by weakness and paralysis
• Nausea and vomiting mediated via the autonomic
ganglia
í/-Tubocurarine is a competitive antagonist of nicot-
inic transmission.
III. TOXIDROMES
Having reviewed the autonomic nervous system, it is
now possible to understand how a drug, or toxin, or
functional class of drugs might mediate a recognisable
constellation of symptoms if it were to serve a role of
agonist or antagonist at one or more of the receptors in
this system. Similarly, drugs which serve as agonists at
opiate receptors also cause a discernible pattern of
response.
Withdrawal from ethanol or other drugs has also
been called a toxidrome. In reality it differs little from
the toxidrome caused by a sympathomimetic agent.
This is due to the fact that withdrawal is accompanied
by an outpouring of sympathetic tone from the central
nervous system. The clinical context provided by hi-
story would be necessary in deciding between these two
(withdrawal and toxicity from a sympathomimetic
agent).
A. Sympathetic Toxidrome
The Sympathetic Toxidrome consists of:
• Central nervous system (CNS) excitation (e.g.
agitation, anxiety, tremor, psychosis)
• Headache
• Seizures
• Hypertension
• Tachycardia
• Diaphoresis (not many toxins cause this)
A Iimited list of agents potentially responsible for
this toxidrome includes:
• Cocaine
• Amphetamines
• Phencyclidine
• LSD
• Ephedrine/pseudoephedrine
• Phenylpropanolamine
• Theophylline
• Caffeine
As will be seen below, this syndrome resembles quite
closely the anticholinergic toxidrome, as well as res-
embling that of alcohol withdrawal as already discus-
sed. There are, however, subtle differences which per-
mit distinctions based on clinical grounds:
• A sympathomimetic agent causes diaphoresis and
little change in bowel motility as assessed by bowel
auscultation (sounds).
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