Pesticide Ingestion - Essay Example

"Pesticide Ingestion" is an engrossing example of a paper on poisoning, toxicology, and environmental health.

Subjective

Observations

Possible physiological explanations

Altered consciousness

Inability to move

Vomiting

Urination(indicated by the wet patch on the bed)

A result of the depression of the central nervous system either caused by chemical changes in the circulation or physical damage to the nervous system.

A musculoskeletal problem or a neuronal problem could manifest as an inability to move.

Vomiting is triggered by the activation of the “vomiting center” in the reticular formation of the medulla oblongata which could either be due to chemoreceptor activation caused by chemical changes in the circulatory system or by irritation of the mucosa of the upper gastrointestinal tract.

Urination is caused by the contraction of the smooth muscle of the bladder (detrusor) triggered by activation of the parasympathetic nerves innervating the detrusor.

Objective observations

Possible physiological explanations

Labored respiration

Drooling

RR=8/pm

Bradycardia (Pulse rate=45bpm)

ON AUSCULTATION

Thoracic rhonchi

Increased abdominal sounds

Paralysis of respiratory muscles causes labored respiration. The attempt to use accessory muscles of respiration for compensation too will manifest as laborious breathing.

Excessive secretion of the salivary glands manifests as drooling and is caused by parasympathetic stimulation.

The respiratory rate may fall as a result of the depression of the respiratory pathways located in the medulla pons and cerebral cortex or as a result of neuromuscular failure inhibiting the act of inhalation and exhalation.

Activation of the parasympathetic nerves innervating the heart (vagi) leads to bradycardia.

Rhonchi are caused by the passage of air through partially obstructed airways. The obstruction could be due to mucosal swelling, secretions or tumor tissue pressing on the passage.

Increased abdominal sounds are caused by excessive gastric motility and secretions caused by cholinergic stimulation of the gastrointestinal tract.

Differential diagnosis

Supporting or refuting information

Organophosphate poisoning

The ketokil that the patient is suspected to have ingested is an organophosphate. Organophosphates irreversibly inhibit the acetylcholinesterase enzyme leading to the accumulation of acetylcholine at muscarinic receptors and nicotinic receptors.

The effect on the muscarinic endings lead to symptoms of cholinergic stimulation (ex. Bradycardia, increased salivation, vomiting, bronchoconstriction, increased respiratory secretions)

The effect on nicotinic receptor endings located at the motor endplate of skeletal muscles leads to fasciculations followed by paralysis of muscle manifested as an inability to move and respiratory discomfort.

Nicotinic receptors of autonomic ganglia are also affected.

Upon exposure to an organophosphate agent, the clinical syndrome progresses through three clearly defined phases: initial cholinergic phase, intermediate syndrome and delayed polyneuropathic phase.

The initial cholinergic phase lasts from 24-48 hours post-exposure and is a medical emergency. Death usually occurs as a result of cardiac effects and respiratory depression.

Within the first 48 hours, the administration of Atropine, a muscarinic antagonist, is effective at countering the initial cholinergic effects. Oximes that are cholinesterase reactivators may be helpful if administered before the cholinesterase organophosphate enzyme complex ages. These should be accompanied by decontamination and airway support and ventilation.

Neostigmine, physostigmine, and diisopropyl phluorophosphate may produce similar symptoms to those of organophosphate poisoning.

Heroine if taken in excess may result in respiratory distress.