Pesticides

Suad Said Al-Bulushi

Rules:• Simple• 2 teams :Team A; R1,R2,R3• Team B; R4,R5• With each Qs; 1 person from each group will

answer, group answer not acceptable & the punishment will be not given them the points, any person from the other team answered without permission (- 10 points )

• If any team could not answer rightly after 2 trials, the q will be shifted to the 2nd team

• Let us learn & enjoy the game ( in order please)

Double JeopardyWhat is

happening?Remember

meFalse or

TrueThink wisely Look closely

20 20 20 20 20

40 40 40 40 40

60 60 60 60 60

80 80 80 80 80

100 100 100 100 100

24 years old gentleman, WT lifter presented to the Ed with hyperthermia & acidosis, after routine cooling rehydration& supportive measures he continued to have persistent hyperthermia with the acidosis which of those is the most likely causative agent?

1)Organophosphate2)Carbamate3)Chlorinated hydrocarbons4)DNP5)(2,4-D)6)2,4,5-T7)Paraquat8)Diquat9)Pyrthrins, or pyrthroids10)Roundup11)DEET12)sympthatomemtics

Regarding Chlorinated hydrocarbon which is true ,& which is false?

1)They affect primarily axonal membranes ,resulting in neuronal irritability & excitation

2)Elimination of some of them can be increased by cholestyramine 40 gram orally every 8 hours

3)The first sign of toxicity may be the acute onset of seizure without peripheral signs & symptoms

4)Seizure activity is usually non self limiting lasting 1-2 weeks

5)Ventricular dysrhythmia are most likely to occur during seizure activity due to high circulating catecholamines & other metabolic abnormalities

A38 y old farm worker presents to the ED with hypersalivation, urinary incontinence, diarrhea, & muscle weakness after being in a recently sprayed field. He has prominent wheezing & is producing copious amounts of clear sputum. Which of the following statements is TRUE of the treatment for this condition?

1)Atropine should be administered as 1 mg IV every 5 mints until muscle weakness has resolved2)Supportive care is the only appropriate treatment for this condition3)Pralidoxime will regenerate cholinesterase molecules if given any time after exposure4)Atropine & Pralidoxime work synergistically to treat this condition

*The pt is having symptoms of cholinergic crisis evidenced by the symptoms given, as well as his recent exposure to the sprayed field, it is unknown exactly whether the agent is organophosphate or carbamate.While both agents inhibit cholinesterase, thus causing accumulation of Ach in neurons of CNs, & autonomic as well as NMJ, organophosphate do so irreversibly. *Atropine & pralidoxime are the two main antidote used for these types of pts . Atropine should be given to adult every 5 mint until muscrininc effects are reversed. Atropine has no effect on muscle weakness.*Pralidoxime acts by regenerating phosphorylated ach –cholinesterase & may also directly detoxify free organophosphate molecules if given as early as within the first 48 hours of ingestion. Its use with atropine appears to be

synergistic .

• A 30-year-old migrant worker drank from a soda can that had been filled with an unknown farm chemical.He is awake, but had to be carried in by his friends. Physical examination is remarkable for pinpoint pupils,wheezing, salivation, dysarthria, and marked generalized muscle weakness. Choose the correct statement:

a. The patient is demonstrating a sympatholytic syndrome of poisoning.

b. You should administer atropine in a dose of 2 mg intravenously every 15 minutes to a maximum total dose of 6 mg or until mydriasis occurs.

c. Urinary alkalinization will increase the elimination of the poison.

d. You should administer pralidoxime (2-PAM) intravenously with a loading dose of 1 g over 15 minutes then at0.5 g/h.

e. Sinus tachycardia should prompt you to decrease the rate of an atropine infusion.

• The patient described is exhibiting cholinergic toxicity probably from the ingestion of an organophosphate or carbamate.

• The first rule in management of organophosphate poisoning is to maintain a patent airway ,Upper airway obstruction from vomitus and copious secretions may occur.,Increased airway resistance from bronchospasm may prove to exceed the respiratory capacity of the weakened muscles of respiration. Hypoxia rapidly ensues from bronchospasm and increased bronchial secretions.

• Early intubation is paramount in treating the poisoning. • The most common cause of treatment failure in severe organophosphate

poisoning is inadequate atropinization.

•The end-point of atropine administration is when drying of secretions occur.• Tachycardia after organophosphate poisoning may be secondary to excessive atropinization necessitating a lower infusion rate,Hypoxia caused by increased pulmonary secretions may also produce tachycardia necessitating a higher infusion rate of atropine. •2-PAM should be given early based on the suspicion of cholinesterase poisoning. It is effective in reversing muscle weakness (nicotinic effects) but only if given within 36 hours of exposure. •2-PAM will reactivate acetylcholinesterase by displacing the organophosphate. Because true cholinesterase regenerates at a rate of only 1% a day, it can take months for symptoms to resolve if cholinesterase is not regenerated with 2-PAM.

• Choose the true statement regarding cholinesterase intoxication with organophosphates or carbamates:

a. Low plasma cholinesterase activity is pathognomonic for organophosphate intoxication.

b. Carbamate poisoning is typically less severe than organophosphate poisoning but presents with marked CNS symptoms.

c. Clinical relapses from organophosphate poisoning may occur for months after an apparent recovery from an acute episode.

d. Bradycardia is a universal finding in clinically important organophosphate poisoning; its absence should prompt an alternative diagnosis.

e. The most common cause of death is cardiac failure.

• Symptoms in organophosphate poisoning may persist for weeks to months as a result of the slow regeneration time for cholinesterase and intermittent mobilization of tissue stores of these lipophilic toxins.•Carbamate poisoning is less severe and CNS symptoms are uncommon because, unlike the organophosphates, these agents do not cross the blood–brain barrier.•Cholinergic effects do not always predominate, since organophosphates also have nicotinic effects.

•The typical pattern following intoxication is tachycardia, followed bybradycardia, AV blocks, and a prolonged QT interval. •The most common cause of death is respiratory failure.

•Low plasma (pseudo) cholinesterase activity is found in a variety of other conditions besides cholinesterase poisoning, including malnutrition, infections, and liver disease. RBC (true) cholinesterase is a more specific but less sensitive measure of poisoning.

Which one of those is false regarding organophosphate toxicity?

1)PTs presenting with no or only metabolic acidosis have higher mortality than those presenting with respiratory or mixed acidosis2)Oxime therapy is indicated in respiratory depression ,fasciculation ,seizures, arrhythmias, cardiovascular instability or needed > (2-4 mg) of atropine3)Sarin, Soman, tabun &VX are nerve agents which differ than household organophosphate insecticides in ageing more quickly 4)Salivation, lacrimation , Urinary incontinence, defection, GI cramps ,Emesis ,Bronchospasm are some of the symptoms caused by its toxicity.

•Regarding DEET toxicity? Which one is true?

1)If DEET exposure is suspected the skin should be thoroughly decontaminated with oil

2)After DEET ingestion the pt should take milk or oil containing food

3)DEET should not be used for infants younger than 2 months old

4)DEET should be applied over abraded row skin

24 years old gentleman, WT lifter presented to the Ed with hyperthermia & acidosis, after routine cooling rehydration& supportive measures he continued to have persistent hyperthermia with the acidosis which of those is the most likely causative agent?1)Organophosphate2)Carbamate3)Chlorinated hydrocarbons4)DNP5)(2,4-D)6)2,4,5-T7)Paraquat8)Diquat9)Pyrthrins, or pyrthroids10)Roundup11)DEET

Regarding Roundup ?

1)Most of its exposure happens through ingestion due to its poor skin absorption

2)The critical elements in diagnosis is history of ingestion

3)Both hydrofluoric acid ingestion & Roundup have the clinical findings of hyperkalemiea & AG metabolic acidosis

4)Ionized Ca level will be low

*In case of sever toxicity with this substance what ECG changes would u see?*Cause of its toxicity?*Mention 3 Negative prognostics indicators?

One statement is false which one is it?

1) RBC cholinesterase level recovers at a rate of 4 % per day in untreated pts with organophosphate toxicity

2) Plasma cholinesterase level may recover in 4- 6 weeks

3) Care givers should use universal precautions including eye shield , protective clothing, & nitrile or butyl rubber gloves in cases or organophosphate exposure

4) Benzodiazepines can be used for controlling agitations, seizure, & coma, after air way has been secure in organophosphate toxicity

Regarding Pyrethrins & pyrthroids?

1)MOST of them are absorbed int the fat ,so cumulative toxicity form problem2) Addtion of piperonyl butoxide reduce their toxicity3)Both of them cause allergic reactions4)They affect sodium channel mediated & GABA Calcium channels

Which of those matches are right:1)Paraquat ,,,,,,,,,,,,,kidney

2)Diquat ,,,,,,,,,,,,,,,,lung

3)(2,4-D),,,,,,,,,,,,,,,,,,,,,,,,,,, skeletal muscles

4)Organophosphate,,,,,,,,,,,,,, carcinogenic

Which is true which is false:

1) Cholinesterase inhibitor include bradycardiea or tachycardia , hypotension or hypertension, miosis or mydriasis2)In chlorinated hydrocarbon exposure catecholamine is avoided3)Rapid cooling & substrate provision (glucose) are the most important therapies in substituted phenol toxicity

*What is this, for what used?*What is the recommended concentration to be used in children?* Mention 3 factors that can increase its toxicity?

1) Mention diagnostic strategies of DNP (at least 3)?one of is highly suggestive?

1) Mention 3 clinical pictures with DNP toxicity predict high likely of complications?

Which is true regarding Bipyrindal compounds?

1)Diquat is poorly absorbed through the skin

2) Paraquat induced pulmonary injury usually occurs over 1- 3 weeks

3)Successful therapeutic intervention for paraquat toxcictry is extremely time dependant & pt outcome depends on the history4)ALL pts with ingested paraquat requires hospitalization

5)All of the above6) Non of the above

*Mention 3 clinical features of DNP toxicity?

* what is characteristic about the site of skin or mucus absorption?

*What is this? which group?*what is its target organ of toxicity & why?

*To which group I belong??*Target organ affected?* When the serious toxic effect develop?

*what is this?*With which group of pts they can get it ? in which group of people ?reversible or not

*What are theses ? What insecticides are extracted from them? How?*what is there predominant form of toxicity? * counseling?

Cute ,but toxic !!!

*What is this? For what purpose it is used?

*Mechanism of toxicity?

Insert Text for QuestionCategory 5 – 100 points

*Which sort of insecticides is this ?For what it is used?*Mechanism of toxicity ?*Best drugs for Dysrhythmia causes by it?