Pharmacokinetics and metabolism
In medical practice, the substance is used as a salt — atropine sulfate. As a drug for the treatment of parkinsonism, it is significantly inferior to modern central muscarinic antagonists (trihexyphenidyl and biperiden) because it causes too many undesirable peripheral adverse reactions.
- Routes of administration: orally (per os) 30–40 minutes before a meal, parenterally, or topically (as eye drops).
- Absorption and distribution: the drug is well absorbed from the intestine. Due to its high lipophilicity, it crosses the blood-brain barrier within 30–60 minutes and accumulates in the CNS.
- Biotransformation: metabolized in the liver via hydrolysis, breaking down into inactive components: tropine and tropic acid.
- Elimination: the half-life is about 2 hours. From 30% to 50% of the substance is excreted unchanged in the urine.
When taken orally, the duration of the therapeutic effect lasts from 4 to 6 hours.
Side effects and contraindications
All adverse reactions of atropine are a pharmacodynamic continuation of its primary action—systemic blockade of muscarinic receptors in various organs. Contraindications for its use strictly stem from these effects.
- Visual system: causes cycloplegia, impairing near vision (the patient cannot focus on close objects). Since the drug increases intraocular pressure, it is strictly contraindicated in glaucoma.
- Cardiovascular system: by blocking vagal influences, atropine causes pronounced tachycardia. Contraindicated in tachyarrhythmias.
- Gastrointestinal tract: simultaneously decreases the tone and peristalsis of intestinal smooth muscle while increasing sphincter tone. This leads to severe obstipation (constipation). Contraindicated in intestinal atony.
- Urinary system: relaxes the bladder wall (detrusor) and causes spasm of the sphincter. Due to the high risk of acute urinary retention, it is contraindicated in benign prostatic hyperplasia (BPH).
- Secretory function: inhibits salivary glands, causing severe dry mouth (xerostomia).
Acute poisoning: clinical presentation
Poisoning most commonly occurs in children who ingest poisonous plants: belladonna (Atropa belladonna), jimsonweed, or henbane. It can also be caused by exceeding the drug dose (including the systemic effect of eye drops) or cross-toxicity with other medications possessing anticholinergic activity (amitriptyline, imipramine, chlorpromazine).
The clinical presentation is divided into two large groups of symptoms:
- Peripheral disorders: persistent pupil dilation (mydriasis), photophobia, blurred vision. Due to the lack of lacrimal fluid, there is a sensation of "sand in the eyes." Severe thirst, dryness of the oral mucosa and throat, speech and swallowing disorders (dysphagia) are observed. The skin becomes flushed (hyperemia), and hyperthermia occurs—in children, body temperature can reach 42 °C due to sweat gland blockade. Pronounced tachycardia (160–190 bpm), extrasystoles, and a risk of myocardial ischemia are recorded by the heart. Bladder atony is possible.
- Central nervous system disorders: motor and mental agitation predominate in the initial stage. "Atropine psychosis" develops—visual and auditory hallucinations, severe anxiety, delirium, coordination and memory impairment. Seizures are possible. In the terminal stage, psychosis is replaced by CNS depression and coma. Death results from respiratory center paralysis.
Principles of poisoning treatment
To save the patient, a comprehensive approach is used, including antidote, detoxification, and symptomatic therapy.
- Antidotes (pathogenetic therapy): anticholinesterase drugs capable of crossing the blood-brain barrier (physostigmine, galantamine) are administered. They increase the concentration of endogenous acetylcholine, which competitively displaces atropine from its receptor binding.
- Removal of the poison (detoxification): gastric lavage with potassium permanganate solution, administration of activated charcoal and saline laxatives. Tannin or strong tea is used to bind alkaloids. In severe cases, active detoxification methods are used: hemoperfusion and forced diuresis.
- Symptomatic care: diazepam or short-acting barbiturates are used to relieve psychomotor agitation. In case of respiratory depression, the patient is transferred to mechanical ventilation.
Belladonna preparations (Belladonna)
Belladonna extracts (dry and thick) and tinctures contain atropine as the main active ingredient. They belong to the group of antispasmodics and are prescribed for painful spasms of the smooth muscles of the gastrointestinal tract and biliary tract.
There are a large number of combination belladonna preparations:
- Tablets: Becarbon, Besalol, Bepasal, Bellalgin.
- Suppositories: Bitiol, Anuzol.
- Drops: Zelenin drops.
Briefly: answers to topical questions
In which diseases is atropine contraindicated?
Atropine is contraindicated in a number of conditions due to the risk of worsening their course. The main contraindications include:
- Glaucoma — the drug increases intraocular pressure.
- Benign prostatic hyperplasia (BPH) — creates a risk of acute urinary retention due to decreased detrusor tone.
- Cardiovascular pathologies — contraindicated in tachyarrhythmias.
- Gastrointestinal pathologies — must not be used in intestinal atony.
Which drugs exhibit cross-toxicity with atropine?
Atropine exhibits cross-toxicity with other medications possessing anticholinergic activity:
- tricyclic antidepressants — imipramine and amitriptyline;
- neuroleptics — chlorpromazine.
What short-acting synthetic substitutes for atropine exist for use in ophthalmology?
In ophthalmology, muscarinic antagonists that have a shorter duration of action on the eye compared to atropine are used:
- homatropine — duration of action 15–20 hours;
- cyclopentolate — duration of action 20–24 hours;
- tropicamide.
For quick memorization of atropine poisoning symptoms, a classic saying is often used: "Blind as a bat (cycloplegia and mydriasis), dry as a bone (inhibition of glandular secretion), red as a beet (skin hyperemia), hot as a hare (hyperthermia), and mad as a hatter (atropine psychosis, delirium, and hallucinations)."
Class and exam questions
Why does atropine poisoning cause a sensation of "sand in the eyes"?
This occurs due to the systemic blockade of muscarinic receptors, leading to a sharp decrease in tear secretion. The cornea and conjunctiva dry out.
What is the mechanism of constipation development during atropine intake?
The drug relaxes the smooth muscle of the gastrointestinal tract, decreasing intestinal tone and peristalsis, while paradoxically increasing sphincter tone, thereby blocking the progression of food contents.
What is the cause of death in severe overdose?
Death occurs due to paralysis of the respiratory center. In the terminal stage of poisoning, severe CNS excitation is replaced by profound depression and coma.
What else to study on this topic
- Central muscarinic antagonists: pharmacology of trihexyphenidyl and biperiden
- Cross-toxicity with tricyclic antidepressants and neuroleptics
- Mechanism of development of cycloplegia and increased intraocular pressure
- Anticholinesterase agents: how physostigmine and galantamine work as antidotes
- Toxicology of plant poisons: alkaloids of jimsonweed and henbane
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