Organophosphate Poisoning
Ingestion of organophosphate compounds presents a significant risk to patients and the health care professionals. Organophosphate poisoning can cause permanent damage it may even result in death (Curtis, Ramsden, Friendship, 2007). Patients who intentionally self harm with the ingestion of organophosphates are usually severely poisoned compared to those who accidently or have occupational exposures. This paper will discuss the case study of Joe (a fictitious name will be used for the purpose of this case study), the pathophysiology to a cellular level relating signs, symptoms and initial collaborative management in relation to the case study outlined in appendix one.
Organophosphate poisoning essentially affects transmission of impulses at the neuromuscular junction (Porth, 2002). Transmission of impulses at the neuromuscular junction is mediated by the release of the neurotransmitter actycholine at pre- and post ganglionic parasympathetic, and pre- ganglionic sympathetic and somatic nerves (Murray, Daly, Little, Cadogan, 2007). Acetylcholine binds to specific receptors of the end plate region of the muscle fiber surface resulting in muscle contraction. Porth states studies “suggest there are more than one million binding sites per motor end-plate”. Acetylcholine Active for only a brief period of the action potential that then generates innervation of the muscle cell. Some of the neurotransmitter diffuses from the synapse; the transmitter that remains is inactivated by an enzyme called acetylchollinesterase. The enzyme splits the acetylcholine molecule into choline and acetic acid. The choline is reused in the synthesis of acetylcholine in the nerve terminal. The rapid inactivation of acetylcholine allows repeated muscle contraction and contractile force.
Organophosphates inhibit acetylcholinesterase enzymes (AChE), cholinergic syndrome occurs when there is an increase acetycholine (Ach) concentration at the central and peripheral muscarinic and
Organophosphate poisoning essentially affects transmission of impulses at the neuromuscular junction (Porth, 2002). Transmission of impulses at the neuromuscular junction is mediated by the release of the neurotransmitter actycholine at pre- and post ganglionic parasympathetic, and pre- ganglionic sympathetic and somatic nerves (Murray, Daly, Little, Cadogan, 2007). Acetylcholine binds to specific receptors of the end plate region of the muscle fiber surface resulting in muscle contraction. Porth states studies “suggest there are more than one million binding sites per motor end-plate”. Acetylcholine Active for only a brief period of the action potential that then generates innervation of the muscle cell. Some of the neurotransmitter diffuses from the synapse; the transmitter that remains is inactivated by an enzyme called acetylchollinesterase. The enzyme splits the acetylcholine molecule into choline and acetic acid. The choline is reused in the synthesis of acetylcholine in the nerve terminal. The rapid inactivation of acetylcholine allows repeated muscle contraction and contractile force.
Organophosphates inhibit acetylcholinesterase enzymes (AChE), cholinergic syndrome occurs when there is an increase acetycholine (Ach) concentration at the central and peripheral muscarinic and