Organophosphates Poisoning

B i.e. Plasma cholinesterase level

B i.e. Edematous lung

C i.e. Tachycardia

A i.e. Pupillary dilation

Ans. is ‘b’ i.e., Esteratic site of AchEs

1. Acetylcholinesterase has two sites:

i)         Catalytic or esteratic site –9 Active site

ii)       Anionic site

• It is quite obvious that to inhibit the action of acetylcholinesterase the active site has to be inhibited and it is esteratic site:

i)        Organophosphates phosphorylate esteratic site.

Carbamates carbomylate esteratic site.

Ans. is ‘a’ i.e., Atropine

Pharmacological treatment of organonhosphatepoisoning

Atropine

o Atropine is the mainstay of treatment (antidote of choice).

o Atropine antagonizes the muscarinic parasympathetic effects of organophosphate (excessive secretion and vasodilation), but does not antagonize nicotinic effects, i.e., neuramuscular blockers (Atropine blocks muscarinic receptors, i.e., it is an antimuscarinic)

o Atropine antagonizes both peripheral as well as central nervous system effects of organophosphates. Cholinesterase regenerator compounds (oximes)

o Pralidoxime is most commonly used oxime.

o Unlike atropine, they antagonize both muscarinic and nicotinic effects.

o They antagonize only peripheral effects, but not central effects except for diacetylmonoxime (DAM) which crosses BBB and antagonizes central effects also.

Ans. is ‘d’ i.e., Is a competitive antagonist of acetylcholine

o Atropine acts as competitive antagonist at muscarinic receptors. It has no activity on nicotinic receptors and has nothing to do with Ach release.

Ans. is ‘c’ i.e., Acts on central and peripheral cholinergic receptors

o In organophosphate poisoning, atropine counteracts the peripheral muscarinic symptoms and at higher doses central effects as well.

o Atropine does not reverse nicotinic action i.e., peripheral muscular paralysis.

Ans. is ‘c’ i.e., Propoxur 

Ans. is `a’ i.e., Dieldrin

Ans. B i.e. Dilated pupil

Ans. C i.e. PAM

• Current antidotes for OP poisoning consist of a pretreatment with carbamates to protect AChE from inhibition by OP compounds and post-exposure treatments with anti-cholinergic drugs.
• Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE.
• Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime)

Ans. A: Physostigmine

The mainstays of medical therapy in organophosphate (OP) poisoning include ‑

• Atropine-arrests muscarinic effects,
• Pralidoxime (2-PAM)-acts by competing for the phosphate moiety of the organophosphorus compound and release it from the cholinesterase enzyme
• Benzodiazepines (e.g., diazepam)-For convulsions

Intravenous glycopyrrolate or diphenhydramine may provide an alternative centrally acting anticholinergic agent used to treat muscarinic toxicity if atropine is unavailable or in limited supply

Ans: A i.e. Heart rate

In organophosphate poisoning, atropine should be administered in doses of 0.6-2 mg i.v., repeated every 10-25 minutes until secretions are controlled, the skin is dr./ and there is sinus tachycardia.

Ans. Diethyltoluamide (DEET)

Ans. Endrin

Ans. Mydriasis

Ans. Late onset proximal myopathy

Ans. Intermediate syndrome

Ans. is ‘c’ i.e., Symptomatic treatment 

• Paralysis due to organophosphate (OP) poisoning can be three types ‑

1. Type I (cholinergic phase)

• It involves acute paralysis secondary to persistent depolarization at the neuromuscular junction caused by persistent stimulation by excessive Ach.
• Treatment of choice is atropine with or without oximes.

2. Type II

• It is also called as intermediate syndrome.
• It develops 1-4 days after resolution of acute cholinergic symptoms.
• It is manifested as paralysis and respiratory distress.
• It involves proximal muscles with relative sparing of distal muscle groups.
• The pathogenesis presumed to be dysfunction of neuromuscular junction caused by downregulation of presynaptic and postsynaptic nicotinic receptors due to release of excessive Ach and Ca’ respectively.
• Atropine is ineffective, symptomatic treatment is given.

3. Type III

• It involves OP-induced delayed polyneuropathy (OPIDN).
• It occurs 1-3 weeks after exposure and is associated with demyelination of axons.
• It is not caused by cholinesterase inhibition but rather by neuropathy target esterase (NTE) inhibition.
• It involves distal muscles with relative sparing of neck muscles, cranial nerves, and proximal muscles.