Podcast
Questions and Answers
How do chemical insecticides primarily affect the target organisms?
How do chemical insecticides primarily affect the target organisms?
- By inhibiting their respiratory systems
- By blocking their digestive systems
- By poisoning their nervous systems (correct)
- By interfering with their reproductive systems
Which of the following is a potential site of action of insecticides?
Which of the following is a potential site of action of insecticides?
- Interference with membrane transport of sodium, potassium, calcium, and chloride ions (correct)
- Enhancement of selective enzymatic activities
- Facilitation of ion transport through nerve endings
- Promotion of neurotransmitter release at muscle endings
What is a possible effect of insecticides on nerve endings?
What is a possible effect of insecticides on nerve endings?
- Decrease in production of neurotransmitters
- Neutral effect on neurotransmitter activity
- Increase in release and/or persistence of neurotransmitters (correct)
- Stimulation of new neurotransmitter pathways
What is a common potential action of classes of insecticides on the nerve axon and terminal portions?
What is a common potential action of classes of insecticides on the nerve axon and terminal portions?
What contributes to the persistence of organochlorine insecticides in the environment?
What contributes to the persistence of organochlorine insecticides in the environment?
Which class of insecticide includes DDT and its analogues?
Which class of insecticide includes DDT and its analogues?
What characteristic makes organochlorine insecticides chemically stable?
What characteristic makes organochlorine insecticides chemically stable?
Which compound belongs to the class of hexachlorocyclohexanes?
Which compound belongs to the class of hexachlorocyclohexanes?
What is the primary metabolite of DDT in humans?
What is the primary metabolite of DDT in humans?
Where are the highest concentrations of DDT found in the body?
Where are the highest concentrations of DDT found in the body?
How is DDT excreted from the body?
How is DDT excreted from the body?
Which isomer of DDT is responsible for its insecticidal activity?
Which isomer of DDT is responsible for its insecticidal activity?
Which mechanism describes the alteration of porous channels through which sodium ions pass?
Which mechanism describes the alteration of porous channels through which sodium ions pass?
What effect does DDT have on the ability of calmodulin to transport calcium ions?
What effect does DDT have on the ability of calmodulin to transport calcium ions?
What role do neuronal adenosine triphosphatases (ATPase) play in neuronal repolarization?
What role do neuronal adenosine triphosphatases (ATPase) play in neuronal repolarization?
How does DDT's reduction of potassium transport across the membrane impact neurons?
How does DDT's reduction of potassium transport across the membrane impact neurons?
What is one of the proposed sites of action of DDT?
What is one of the proposed sites of action of DDT?
How does DDT potentially affect the transport of potassium?
How does DDT potentially affect the transport of potassium?
What is a suggested effect of DDT on calmodulin-calcium binding?
What is a suggested effect of DDT on calmodulin-calcium binding?
Which of the following is a potential site of action of DDT?
Which of the following is a potential site of action of DDT?
Which of the following is the earliest symptom of poisoning by DDT in humans?
Which of the following is the earliest symptom of poisoning by DDT in humans?
What is the primary target for DDT toxicity based on the signs and symptoms of acute poisoning?
What is the primary target for DDT toxicity based on the signs and symptoms of acute poisoning?
According to animal data, how is DDT classified in terms of its potential impact on humans?
According to animal data, how is DDT classified in terms of its potential impact on humans?
Which organ or system is considered an important target for DDT in chronic exposure?
Which organ or system is considered an important target for DDT in chronic exposure?
Which class of organochlorine insecticides includes compounds that antagonize the action of the neurotransmitter GABA?
Which class of organochlorine insecticides includes compounds that antagonize the action of the neurotransmitter GABA?
What is the γ isomer of benzene hexachloride known as?
What is the γ isomer of benzene hexachloride known as?
Which compound is rapidly metabolized to dieldrin?
Which compound is rapidly metabolized to dieldrin?
What is the primary mechanism of neurotoxic action shared by the hexachlorocyclohexanes and cyclodiene insecticides?
What is the primary mechanism of neurotoxic action shared by the hexachlorocyclohexanes and cyclodiene insecticides?
What is the mechanism of action shared by hexachlorocyclohexanes and cyclodiene insecticides?
What is the mechanism of action shared by hexachlorocyclohexanes and cyclodiene insecticides?
Which compound is the γ isomer of benzene hexachloride?
Which compound is the γ isomer of benzene hexachloride?
Which class of insecticides includes chlordane, dieldrin, and aldrin?
Which class of insecticides includes chlordane, dieldrin, and aldrin?
What is the primary mechanism of neurotoxic action for organochlorine insecticides?
What is the primary mechanism of neurotoxic action for organochlorine insecticides?
What is the primary effect of endogenous GABA binding to its receptors?
What is the primary effect of endogenous GABA binding to its receptors?
What is the primary action of Lindane and cyclodienes on the chloride channel?
What is the primary action of Lindane and cyclodienes on the chloride channel?
What is the result of inhibiting Na+,K+-ATPase and Ca2+,Mg2+ ATPase by Class 2 and Class 3 insecticides?
What is the result of inhibiting Na+,K+-ATPase and Ca2+,Mg2+ ATPase by Class 2 and Class 3 insecticides?
What is the primary effect of GABA antagonists like Lindane and cyclodienes on neurotransmission?
What is the primary effect of GABA antagonists like Lindane and cyclodienes on neurotransmission?
What is the primary target for the toxicity of Lindane and cyclodienes?
What is the primary target for the toxicity of Lindane and cyclodienes?
What is the main difference in symptoms of poisoning between DDT and Lindane/cyclodienes?
What is the main difference in symptoms of poisoning between DDT and Lindane/cyclodienes?
What effect do cyclodienes have on the liver upon chronic exposure?
What effect do cyclodienes have on the liver upon chronic exposure?
Where do Lindane and cyclodienes tend to bioaccumulate?
Where do Lindane and cyclodienes tend to bioaccumulate?
What is the primary target for the toxicity of Lindane and cyclodienes?
What is the primary target for the toxicity of Lindane and cyclodienes?
What is a prominent aspect of poisoning by Lindane and cyclodienes?
What is a prominent aspect of poisoning by Lindane and cyclodienes?
What is the effect of cyclodienes on the liver upon chronic exposure?
What is the effect of cyclodienes on the liver upon chronic exposure?
Where do Lindane and cyclodienes tend to bioaccumulate?
Where do Lindane and cyclodienes tend to bioaccumulate?
What is the primary manifestation of chlordecone toxicity?
What is the primary manifestation of chlordecone toxicity?
What is believed to be the mechanism of chlordecone neurotoxicity?
What is believed to be the mechanism of chlordecone neurotoxicity?
What effect does chlordecone have on the liver?
What effect does chlordecone have on the liver?
What reproductive effect has been observed in chlordecone-exposed workers?
What reproductive effect has been observed in chlordecone-exposed workers?
Which of the following best defines an endocrine disruptor?
Which of the following best defines an endocrine disruptor?
Which compound has estrogenic properties and can act as an agonist at estrogen receptors?
Which compound has estrogenic properties and can act as an agonist at estrogen receptors?
What is the primary negative effect of the metabolite p,p-DDE on androgen receptors?
What is the primary negative effect of the metabolite p,p-DDE on androgen receptors?
Which category of insecticides includes compounds with weak estrogenic activity?
Which category of insecticides includes compounds with weak estrogenic activity?
What is the definition of an endocrine disruptor?
What is the definition of an endocrine disruptor?
What is the primary mechanism of action of the o,p-isomer of DDT?
What is the primary mechanism of action of the o,p-isomer of DDT?
Which compound has estrogenic properties and can act as an agonist at estrogen receptors?
Which compound has estrogenic properties and can act as an agonist at estrogen receptors?
What do organochlorine compounds with weak estrogenic activity primarily affect?
What do organochlorine compounds with weak estrogenic activity primarily affect?
How does the oral administration of anion-exchange resin (cholestyramine) affect the fecal excretion of chlordecone?
How does the oral administration of anion-exchange resin (cholestyramine) affect the fecal excretion of chlordecone?
What is the rationale for the use of cholestyramine in increasing fecal excretion of chlordecone?
What is the rationale for the use of cholestyramine in increasing fecal excretion of chlordecone?
What is the primary impact of cholestyramine on the biological half-life of chlordecone?
What is the primary impact of cholestyramine on the biological half-life of chlordecone?
How does cholestyramine potentially reduce chlordecone reabsorption in the intestinal tract?
How does cholestyramine potentially reduce chlordecone reabsorption in the intestinal tract?
What is the primary rationale for using cholestyramine to increase fecal excretion of chlordecone?
What is the primary rationale for using cholestyramine to increase fecal excretion of chlordecone?
What effect does cholestyramine potentially have on chlordecone reabsorption in the intestinal tract?
What effect does cholestyramine potentially have on chlordecone reabsorption in the intestinal tract?
What is the primary impact of cholestyramine on the biological half-life of chlordecone?
What is the primary impact of cholestyramine on the biological half-life of chlordecone?
Where does cholestyramine retain the bound chlordecone to increase fecal excretion?
Where does cholestyramine retain the bound chlordecone to increase fecal excretion?
What is the common mechanism of action shared by the two types of insecticides?
What is the common mechanism of action shared by the two types of insecticides?
What do the esters of phosphoric or phosphorothioic acid and the esters of carbamic acid have in common?
What do the esters of phosphoric or phosphorothioic acid and the esters of carbamic acid have in common?
What is the role of X in the general structure of OP insecticides?
What is the role of X in the general structure of OP insecticides?
What are R1 and R2 in the general structure of OP insecticides typically composed of?
What are R1 and R2 in the general structure of OP insecticides typically composed of?
What is the most sensitive to hydrolysis in the general structure of OP insecticides?
What is the most sensitive to hydrolysis in the general structure of OP insecticides?
Which chemical class of insecticides includes esters of carbamic acid?
Which chemical class of insecticides includes esters of carbamic acid?
What is the common mechanism of action for the agents comprising a type of insecticide ?
What is the common mechanism of action for the agents comprising a type of insecticide ?
What are R1 and R2 in the general structure of OP insecticides primarily composed of?
What are R1 and R2 in the general structure of OP insecticides primarily composed of?
What is the common mechanism of action shared by the two types of insecticides?
What is the common mechanism of action shared by the two types of insecticides?
Which chemical class of insecticides includes esters of carbamic acid?
Which chemical class of insecticides includes esters of carbamic acid?
What contributes to the persistence of organochlorine insecticides in the environment?
What contributes to the persistence of organochlorine insecticides in the environment?
What is the primary impact of cholestyramine on the biological half-life of chlordecone?
What is the primary impact of cholestyramine on the biological half-life of chlordecone?
What is the primary metabolic bioactivation process for compounds containing a sulfur bound to phosphorus?
What is the primary metabolic bioactivation process for compounds containing a sulfur bound to phosphorus?
Which enzymes are primarily responsible for the oxidative desulfuration of compounds containing sulfur bound to phosphorus?
Which enzymes are primarily responsible for the oxidative desulfuration of compounds containing sulfur bound to phosphorus?
What type of analog is formed during the oxidative desulfuration of compounds containing sulfur bound to phosphorus?
What type of analog is formed during the oxidative desulfuration of compounds containing sulfur bound to phosphorus?
Where does the oxidative desulfuration of compounds containing sulfur bound to phosphorus predominantly take place?
Where does the oxidative desulfuration of compounds containing sulfur bound to phosphorus predominantly take place?
What happens to the AChE enzyme following the reaction with an organophosphorus ester?
What happens to the AChE enzyme following the reaction with an organophosphorus ester?
What is the effect of inhibiting Na+,K+-ATPase and Ca2+,Mg2+ ATPase by Class 2 and Class 3 insecticides?
What is the effect of inhibiting Na+,K+-ATPase and Ca2+,Mg2+ ATPase by Class 2 and Class 3 insecticides?
How does DDT's reduction of potassium transport across the membrane impact neurons?
How does DDT's reduction of potassium transport across the membrane impact neurons?
What is the primary impact of GABA antagonists like Lindane and cyclodienes on neurotransmission?
What is the primary impact of GABA antagonists like Lindane and cyclodienes on neurotransmission?
What happens to the AChE enzyme following the reaction with an organophosphorus ester?
What happens to the AChE enzyme following the reaction with an organophosphorus ester?
What is the primary impact of cholestyramine on the biological half-life of chlordecone?
What is the primary impact of cholestyramine on the biological half-life of chlordecone?
What is the common mechanism of action for the agents comprising a type of insecticide?
What is the common mechanism of action for the agents comprising a type of insecticide?
What are R1 and R2 in the general structure of OP insecticides primarily composed of?
What are R1 and R2 in the general structure of OP insecticides primarily composed of?
What is the primary impact of inhibiting AChE by organophosphates (OPs)?
What is the primary impact of inhibiting AChE by organophosphates (OPs)?
What is the primary consequence of AChE inhibition at cholinergic synapses?
What is the primary consequence of AChE inhibition at cholinergic synapses?
What is the primary result of AChE inhibition by organophosphates (OPs) in the body?
What is the primary result of AChE inhibition by organophosphates (OPs) in the body?
What is the consequence of AChE inhibition by organophosphates (OPs) at cholinergic synapses?
What is the consequence of AChE inhibition by organophosphates (OPs) at cholinergic synapses?
What effect can be expected from the stimulation of muscarinic receptors of the parasympathetic autonomic nervous system?
What effect can be expected from the stimulation of muscarinic receptors of the parasympathetic autonomic nervous system?
What is believed to be the primary cause of death when respiratory failure occurs due to exposure to certain substances?
What is believed to be the primary cause of death when respiratory failure occurs due to exposure to certain substances?
Which effect is associated with the action of chlordecone in the intestinal tract?
Which effect is associated with the action of chlordecone in the intestinal tract?
What symptoms can result from the effects of substances on the CNS?
What symptoms can result from the effects of substances on the CNS?
What is the hallmark of severe organophosphate (OP) poisoning?
What is the hallmark of severe organophosphate (OP) poisoning?
Which symptoms are observed most often in mild and moderate OP poisoning?
Which symptoms are observed most often in mild and moderate OP poisoning?
What are the first signs to appear in OP poisoning?
What are the first signs to appear in OP poisoning?
What is a hallmark of severe chlordecone poisoning?
What is a hallmark of severe chlordecone poisoning?
What is the primary means of replacing the activity of irreversibly inhibited AChE?
What is the primary means of replacing the activity of irreversibly inhibited AChE?
What facilitates the dephosphorylation of AChE in the therapy of OP poisoning?
What facilitates the dephosphorylation of AChE in the therapy of OP poisoning?
What is the impact of aging on phosphorylated AChE?
What is the impact of aging on phosphorylated AChE?
What determines the rate of aging of phosphorylated AChE and the need for enzyme replacement?
What determines the rate of aging of phosphorylated AChE and the need for enzyme replacement?
What effect would the presence of P–O–C bonds have on aging ?
What effect would the presence of P–O–C bonds have on aging ?
What type of bonds in P–R would prevent aging ?
What type of bonds in P–R would prevent aging ?
In what form of P-R bonds would aging not be possible?
In what form of P-R bonds would aging not be possible?
What type of P-R bonds are associated with rapid aging?
What type of P-R bonds are associated with rapid aging?
What is the primary feature of the Intermediate Syndrome in organophosphate (OP) poisoning?
What is the primary feature of the Intermediate Syndrome in organophosphate (OP) poisoning?
What is the mortality rate due to respiratory paralysis and complications in the Intermediate Syndrome?
What is the mortality rate due to respiratory paralysis and complications in the Intermediate Syndrome?
What is one hypothesis for the cause of muscle weakness in the Intermediate Syndrome?
What is one hypothesis for the cause of muscle weakness in the Intermediate Syndrome?
What is the primary treatment for the Intermediate Syndrome?
What is the primary treatment for the Intermediate Syndrome?
When does the Intermediate Syndrome typically develop after OP poisoning?
When does the Intermediate Syndrome typically develop after OP poisoning?
What is the usual recovery period in surviving patients with the Intermediate Syndrome?
What is the usual recovery period in surviving patients with the Intermediate Syndrome?
What is a common symptom of Organophosphate-Induced Delayed Polyneuropathy (OPIDP)?
What is a common symptom of Organophosphate-Induced Delayed Polyneuropathy (OPIDP)?
When do the signs and symptoms of Organophosphate-Induced Delayed Polyneuropathy (OPIDP) typically occur?
When do the signs and symptoms of Organophosphate-Induced Delayed Polyneuropathy (OPIDP) typically occur?
What is the primary impact of AChE (Acetylcholinesterase) inhibition by organophosphates (OPs) in the body?
What is the primary impact of AChE (Acetylcholinesterase) inhibition by organophosphates (OPs) in the body?
Which of the following is a sign of Organophosphate-Induced Delayed Polyneuropathy (OPIDP)?
Which of the following is a sign of Organophosphate-Induced Delayed Polyneuropathy (OPIDP)?
What is the necessary percentage of NTE phosphorylation for OPIDP to be initiated?
What is the necessary percentage of NTE phosphorylation for OPIDP to be initiated?
What is the target enzyme for OPIDP?
What is the target enzyme for OPIDP?
Which type of compounds can cause OPIDP?
Which type of compounds can cause OPIDP?
What is the primary impact of organophosphates (OPs) on NTE?
What is the primary impact of organophosphates (OPs) on NTE?
What is the primary reason for the distinctive difference in neurotoxicity action between carbamic acid esters and organophosphates?
What is the primary reason for the distinctive difference in neurotoxicity action between carbamic acid esters and organophosphates?
What distinguishes carbamic acid esters as poor substrates for the cholinesterase enzymes compared to organophosphates?
What distinguishes carbamic acid esters as poor substrates for the cholinesterase enzymes compared to organophosphates?
What distinguishes organophosphates as frequently considered to be irreversible inhibitors of AChE?
What distinguishes organophosphates as frequently considered to be irreversible inhibitors of AChE?
What characterizes the distinct difference in neurotoxic action between carbamic acid esters and organophosphates?
What characterizes the distinct difference in neurotoxic action between carbamic acid esters and organophosphates?
What distinguishes carbamate insecticides from most organophosphorus compounds?
What distinguishes carbamate insecticides from most organophosphorus compounds?
What is the primary difference between the signs and symptoms of acute intoxication by carbamate insecticides and organophosphorus compounds?
What is the primary difference between the signs and symptoms of acute intoxication by carbamate insecticides and organophosphorus compounds?
What is the reason for the extensive toxicologic short-term toxicity following acute administration of carbamate insecticides?
What is the reason for the extensive toxicologic short-term toxicity following acute administration of carbamate insecticides?
What is the primary reason for fatalities occurring in humans due to carbamate insecticide toxicity?
What is the primary reason for fatalities occurring in humans due to carbamate insecticide toxicity?
What is the primary indicator of the severity of organophosphorus ester poisoning?
What is the primary indicator of the severity of organophosphorus ester poisoning?
What immediate action is required in response to life-threatening signs of anticholinesterase poisoning?
What immediate action is required in response to life-threatening signs of anticholinesterase poisoning?
What should be monitored in cases of anticholinesterase poisoning, in addition to the status of the patient?
What should be monitored in cases of anticholinesterase poisoning, in addition to the status of the patient?
What is a consequence of extensive nervous system involvement in anticholinesterase poisoning?
What is a consequence of extensive nervous system involvement in anticholinesterase poisoning?
What is a good indicator of the severity of organophosphorus ester poisoning?
What is a good indicator of the severity of organophosphorus ester poisoning?
What is the immediate action required for life-threatening signs of anticholinesterase poisoning?
What is the immediate action required for life-threatening signs of anticholinesterase poisoning?
What should be monitored as a consequence of the extensive involvement of the entire nervous system in anticholinesterase poisoning?
What should be monitored as a consequence of the extensive involvement of the entire nervous system in anticholinesterase poisoning?
What is the primary indicator of severe organophosphate (OP) poisoning?
What is the primary indicator of severe organophosphate (OP) poisoning?
What is the recommended action for all cases of anticholinesterase poisoning?
What is the recommended action for all cases of anticholinesterase poisoning?
Which enzyme's inhibition is a good indicator of the severity of organophosphorus ester poisoning?
Which enzyme's inhibition is a good indicator of the severity of organophosphorus ester poisoning?
What is required to maintain a patent airway in cases of life-threatening signs in anticholinesterase poisoning?
What is required to maintain a patent airway in cases of life-threatening signs in anticholinesterase poisoning?
What should be monitored as a consequence of the extensive involvement of the entire nervous system in anticholinesterase poisoning?
What should be monitored as a consequence of the extensive involvement of the entire nervous system in anticholinesterase poisoning?
What is the role of diazepam in the treatment of organophosphorus and/or carbamate intoxications?
What is the role of diazepam in the treatment of organophosphorus and/or carbamate intoxications?
What is the antidotal therapy for organophosphorus ester insecticide poisoning usually based on?
What is the antidotal therapy for organophosphorus ester insecticide poisoning usually based on?
What is the primary impact of AChE (Acetylcholinesterase) inhibition by organophosphates (OPs) in the body?
What is the primary impact of AChE (Acetylcholinesterase) inhibition by organophosphates (OPs) in the body?
What characterizes the distinct difference in neurotoxic action between carbamic acid esters and organophosphates?
What characterizes the distinct difference in neurotoxic action between carbamic acid esters and organophosphates?
What is the primary reason for using frequent small doses of atropine in cases of mild signs and symptoms of anticholinesterase poisoning?
What is the primary reason for using frequent small doses of atropine in cases of mild signs and symptoms of anticholinesterase poisoning?
What is the supplementary treatment for moderate to severe nicotinic symptoms in cases of anticholinesterase poisoning?
What is the supplementary treatment for moderate to severe nicotinic symptoms in cases of anticholinesterase poisoning?
What is the primary consequence of AChE inhibition by organophosphates (OPs) at cholinergic synapses?
What is the primary consequence of AChE inhibition by organophosphates (OPs) at cholinergic synapses?
What is the status that must be monitored continuously in cases of anticholinesterase poisoning?
What is the status that must be monitored continuously in cases of anticholinesterase poisoning?
What is the primary requirement for a reactivating molecule for AChE inhibition?
What is the primary requirement for a reactivating molecule for AChE inhibition?
What is the therapeutic action of oxime compounds based on?
What is the therapeutic action of oxime compounds based on?
What contributes to the irreversible inhibition of AChE by organophosphorus esters?
What contributes to the irreversible inhibition of AChE by organophosphorus esters?
What aids in the rapid dephosphorylation of the phosphorylated enzyme?
What aids in the rapid dephosphorylation of the phosphorylated enzyme?
What is the practical limitation on the usefulness of oxime reactivators?
What is the practical limitation on the usefulness of oxime reactivators?
What is the product of the oxime reaction with either the phosphorylated enzyme or with free, unbound organophosphorus ester?
What is the product of the oxime reaction with either the phosphorylated enzyme or with free, unbound organophosphorus ester?
What happens to the phosphorylated enzyme in 'aged' AChE?
What happens to the phosphorylated enzyme in 'aged' AChE?
What is the nature of the reaction between oxime and the phosphorylated enzyme or free, unbound organophosphorus ester?
What is the nature of the reaction between oxime and the phosphorylated enzyme or free, unbound organophosphorus ester?
What should be administered repeatedly over several days if the absorption, distribution, and/or metabolism of the organophosphorus ester is delayed in the body?
What should be administered repeatedly over several days if the absorption, distribution, and/or metabolism of the organophosphorus ester is delayed in the body?
What may alleviate severe muscle cramping, particularly in the extremities, caused by the repeated dosing of pralidoxime?
What may alleviate severe muscle cramping, particularly in the extremities, caused by the repeated dosing of pralidoxime?
What binding by pralidoxime causes muscle spasms similar to those caused by the organophosphorus esters?
What binding by pralidoxime causes muscle spasms similar to those caused by the organophosphorus esters?
What is the primary treatment for severe muscle cramping, particularly in the extremities, caused by repeated dosing with pralidoxime?
What is the primary treatment for severe muscle cramping, particularly in the extremities, caused by repeated dosing with pralidoxime?
What is the primary difference in the clinical treatment of carbamate toxicity compared to organophosphorus ester insecticide intoxication?
What is the primary difference in the clinical treatment of carbamate toxicity compared to organophosphorus ester insecticide intoxication?
What did reports reveal about the use of pralidoxime in treating carbaryl intoxications?
What did reports reveal about the use of pralidoxime in treating carbaryl intoxications?
What is the important consideration regarding the treatment of anticholinesterase-type insecticide intoxications?
What is the important consideration regarding the treatment of anticholinesterase-type insecticide intoxications?
What is the similarity in the clinical treatment of carbamate toxicity and organophosphorus ester insecticide intoxication?
What is the similarity in the clinical treatment of carbamate toxicity and organophosphorus ester insecticide intoxication?
What are pyrethrins?
What are pyrethrins?
Which type of pyrethrins contains the -cyano substituent?
Which type of pyrethrins contains the -cyano substituent?
What is the primary source of pyrethrins?
What is the primary source of pyrethrins?
What distinguishes pyrethrins from carbamate and organophosphorus insecticides?
What distinguishes pyrethrins from carbamate and organophosphorus insecticides?
What impact do pyrethroids have on sodium channels?
What impact do pyrethroids have on sodium channels?
What is the primary difference between type I and type II esters in relation to sodium channels?
What is the primary difference between type I and type II esters in relation to sodium channels?
What is the effect of type II esters on sodium ion transport within neurons?
What is the effect of type II esters on sodium ion transport within neurons?
What is the impact of both type I and type II esters on sodium channels?
What is the impact of both type I and type II esters on sodium channels?
What is the potential effect of inhibiting Ca2, Mg2-ATPase by several agents such as permethrin, cypermethrin, and deltamethrin?
What is the potential effect of inhibiting Ca2, Mg2-ATPase by several agents such as permethrin, cypermethrin, and deltamethrin?
What is the action of Type II esters at relatively high concentrations in the mammalian brain?
What is the action of Type II esters at relatively high concentrations in the mammalian brain?
What is the potential consequence of Type II ester intoxication on seizures?
What is the potential consequence of Type II ester intoxication on seizures?
What is the primary effect of inhibiting GABA-gated chloride channels in the mammalian brain?
What is the primary effect of inhibiting GABA-gated chloride channels in the mammalian brain?
Which compound produces profuse salivation, coarse tremor progressing to clonic seizures?
Which compound produces profuse salivation, coarse tremor progressing to clonic seizures?
What is the primary adverse effect resulting from dermal contact with pyrethroids?
What is the primary adverse effect resulting from dermal contact with pyrethroids?
What is the hallmark of severe organophosphate (OP) poisoning?
What is the hallmark of severe organophosphate (OP) poisoning?
What is the primary impact of GABA antagonists like Lindane and cyclodienes on neurotransmission?
What is the primary impact of GABA antagonists like Lindane and cyclodienes on neurotransmission?
What is the primary reason for fatalities occurring in humans due to pyrethrin poisoning?
What is the primary reason for fatalities occurring in humans due to pyrethrin poisoning?
What does piperonyl butoxide do when included in commercial forms of pyrethrins?
What does piperonyl butoxide do when included in commercial forms of pyrethrins?
What may a patient also exhibit signs of, if pyrethrins are sold in hydrocarbon solution?
What may a patient also exhibit signs of, if pyrethrins are sold in hydrocarbon solution?
What is the primary impact of piperonyl butoxide on the activity of insects?
What is the primary impact of piperonyl butoxide on the activity of insects?
What is the primary concern in organochlorine insecticide poisoning?
What is the primary concern in organochlorine insecticide poisoning?
What is the recommended treatment to control convulsions in organochlorine insecticide poisoning?
What is the recommended treatment to control convulsions in organochlorine insecticide poisoning?
What is the effect of repetitive stimulation of the CNS in organochlorine insecticide poisoning?
What is the effect of repetitive stimulation of the CNS in organochlorine insecticide poisoning?
In addition to general decontamination and supportive treatment, what medication may be administered to control the convulsions in organochlorine insecticide poisoning?
In addition to general decontamination and supportive treatment, what medication may be administered to control the convulsions in organochlorine insecticide poisoning?
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Study Notes
Chemical Insecticides
- Chemical insecticides primarily affect target organisms by interfering with nerve impulses, disrupting ion channels and receptors, and altering enzyme function.
- Potential sites of action include nerve endings, axon and terminal portions, and sodium and calcium channels.
Organochlorine Insecticides
- Organochlorine insecticides, including DDT and its analogues, are chemically stable due to their cyclic structure.
- They persist in the environment due to their low biodegradability and high lipophilicity.
- They can bioaccumulate in fatty tissues and biomagnify up food chains.
DDT
- DDT (dichlorodiphenyltrichloroethane) is an organochlorine insecticide that affects nerve endings, axon and terminal portions, and sodium and calcium channels.
- Its primary metabolite in humans is DDE (dichlorodiphenyldichloroethylene).
- Highest concentrations of DDT are found in fatty tissues, and it is excreted through the bile and feces.
- The insecticidal activity of DDT is attributed to its p,p'-isomer.
- DDT alters the transport of potassium, affecting neuronal repolarization, and binds to calmodulin, altering calcium ion transport.
Hexachlorocyclohexanes
- Hexachlorocyclohexanes, including Lindane (γ-hexachlorocyclohexane), are another class of organochlorine insecticides.
- They antagonize the action of the neurotransmitter GABA, affecting chloride channels and leading to neuronal hyperexcitation.
Cyclodiene Insecticides
- Cyclodiene insecticides, including chlordane and aldrin, are organochlorine compounds that antagonize GABA receptors, affecting chloride channels.
- They are rapidly metabolized to more toxic compounds, such as dieldrin.
Endocrine Disruptors
- Endocrine disruptors, including some organochlorine insecticides, interfere with hormone function, affecting reproductive and developmental processes.
- p,p'-DDE, a metabolite of DDT, has anti-androgenic properties, affecting reproductive health.
- Chlordecone, a cyclodiene insecticide, has estrogenic properties, acting as an agonist at estrogen receptors.
Cholestyramine and Chlordecone
- Cholestyramine, an anion-exchange resin, increases the fecal excretion of chlordecone by binding to it in the gut, reducing reabsorption and increasing elimination.
Organophosphorus Insecticides
- Organophosphorus insecticides, such as malathion and parathion, are esters of phosphoric or phosphorothioic acid.
- They inhibit acetylcholinesterase (AChE), leading to an accumulation of acetylcholine, which overstimulates muscarinic and nicotinic receptors.
- Inhibiting Na+,K+-ATPase and Ca2+,Mg2+ ATPase can lead to neurological and muscular effects.
Toxicity and Symptoms
- Symptoms of poisoning by DDT, Lindane, and cyclodienes include muscle weakness, tremors, and seizures, while chlordecone poisoning can cause tremors, muscle weakness, and liver damage.
- Organophosphate poisoning can cause muscle weakness, fasciculations, and respiratory failure.
- The primary impact of cholestyramine on the biological half-life of chlordecone is to reduce it.
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