Section 8: Pesticides Flashcards
8.1 Given an exposure, identify the insecticide or herbicide that is potentially responsible and
treatment.
8.1 Given an exposure, identify the insecticide or herbicide that is potentially responsible and
treatment.
- Borates and Boric Acid
a. n/v/d.
- emesis and diarrhea may have blue-green color.
b. Erythematous rash
c. Charcoal not very useful
d. Dialysis IS effective
- Carbamates
Ex: aldicarb (Temik), carbofuran (Furadan), carbaryl (Sevin), ethienocarb, fenobucarb, oxamyl, and methomyl
a. SLUDGE and Killer Bs similar to organophosphates.
b. Treatment is atropine for SLUDGE and Killer Bs.
Carbamates do not affect the CNS because they do not cross the blood brain barrier, and they do not cause aging of ACeE
*Consider pralidoxime (2-PAM) in cases of mixed carbamate/organophosphate poisoning
and cases of an unknown pesticide with muscarinic symptoms on presentation. Pralidoxime is probably of little value in N-methyl carbamate poisonings (no aging) and is not indicated in isolated carbamate poisonings. Atropine alone usually is effective.
- Chlorinated Hydrocarbons (i.e. lindane, DDT)
a. Organochlorines
i. MOA
1. Disrupts Na and K channels affecting nerve transmission. Seizures.
2. Antagonizes GABA (hyper-excitable state in CNS and PNS)
ii. Treatment
1. Removal from source
2. Irrigate/wash with soap and water
3. Cholestyramine (nonabsorbable bile acid) to increase fecal elimination
- Benzos for seizures
- Herbicides
a. Chlorophenoxy Compounds (ex 2.4-D)
i. Minor ingestion generally see n/v/abd pain/diarrhea
ii. In large ingestion note muscle weakness with elevated CK.
iii. Is an UNcoupler (hyperthermia)
b. Glyphosate (ex Roundup)
i. In minor ingestion expect irritation of exposed area/system
ii. In large ingestion may see mucosal injury, myocardial depression (may be related to surfactant)
c. Paraquat and Diquat 297
i. Corrosive
ii. Multisystem organ damage
- Neonicotinoids (i.e. imidacloprid)
a. Minor ingestion: n/v/d/mild sedation
b. Large ingestion: sz, acidosis, coma, dysrhythmias
- Pyrethriins, Pyrethroids, and Piperonyl Butoxide
a. Pyrethrins/pyrethroids
- n/v/oral paresthesias
- Ingestions may cause sz, hyperexcitability, coma
8.2 Identify the toxicity and symptoms of exposure to carbamates and organophosphates.
8.2 Identify the toxicity and symptoms of exposure to carbamates and organophosphates.
- Carbamates
a. Ex. Carbaryl (Sevin); Propoxur
b. MOA
i. Block acetylcholine breakdown (competitive inhibition). Increased cholinergic stimulation. Less toxic than organophosphates b/c enzyme action can be
regenerated
– DUMBELS/SLUDGE (muscarinic receptors)
– Fasciculations, weakness, paralysis, tachycardia, HTN (nicotinic receptors)
– Poor CNS penetration (seizures and coma rare)
—- CNS effects are secondary to bronchospasm and bronchorrhea (hypoxia)
4. Treatment
– Atropine (not 2-PAM)
– Remove from source
– Irrigate. Wash with soap and water
– Nondepolarizing paralytic for intubation (vecc or rocc)
Malaise, muscle weakness, dizziness and sweating are commonly reported
early symptoms. Miosis with blurred vision, incoordination, muscle twitching and
slurred speech are reported. Headache, salivation, nausea, vomiting, abdominal pain
and diarrhea are often prominent. Transient hyperbilirubinemia may occur. Acute
pancreatitis has also been reported in some of the cases of aldicarb and methomyl
poisoning. Some cases of pancreatitis have required surgical drainage of a pancreatitic
pseudocyst.
The most severe manifestations of carbamate poisoning occur in the respiratory
and central nervous (CNS) systems. CNS findings include coma, seizures and hypoto-
nicity, and nicotinic effects including hypertension and cardiorespiratory depression.
The respiratory depression also results from skeletal muscle impairment in which
the chest wall cannot expand for adequate respiration. Dyspnea, bronchospasm and
bronchorhea with eventual pulmonary edema are other serious signs.
Carbamates do not affect the CNS because they do not cross the blood brain barrier, and they do not cause aging of ACeE
- Organophosphates
a. Ex. Malathion, Diazinon, Chlorpyrifos
MOA
i. Acetylcholine breakdown inhibited-noncompetative inhibition (excess cholinergic stimulation) ii. DUMBELS/SLUDGE (muscarinic stimulation) iii. fasciculations, weakness, paralysis, sz, tachycardia & HTN (nicotinic stimulation) iv. cardiac starts with tachy/HTN, then heart blocks, then bradycardia, QT prolongation v. resp rhinnorhea, excessive secretions, bronchoconstriction, wheezing, tachypnea, resp depression vi. QT prolongation
- Organophosphates
c. Differentials: nerve agents, carbamate, nicotine poisoning (cholinergic toxidrome)
d. Labs: can check blood levels (PSE) so should be decreased
e. Many organophosphates smell like petroleum or garlic
- Organophosphates
Treatment
i. Remove from source
ii. Irrigate and wash with soap and water
iii. Consider charcoal for ingestion
iv. Non-depolarizing agent for intubation (vecc or rocc)
v. Succs metabolized by AChE which is inhibited by organophosphate toxicity. Will not wear off
vi. Atropine: titrate to dry pulmonary secretions and resolve wheezing
vii. Pralidoxime (prevent aging of AChE receptors)
viii. Benzos to prevent and treat seizures
ix. ECG to assess for QT prolongation
*any comatose OP poisoned patient should be treated w/ benzos AND atropine
8.5 Given a rodenticide exposure, identify the appropriate treatment.
- Various kinds
a. Confirm type of rodenticide and ingredients to determine s/s to watch for
- Super warfarins
a. PT best test to evaluate clotting function
b. May not show anticoagulation until up to 15 hrs after ingestion
c. Consider FFP, whole blood, clotting factors
d. Vitamin K1
- If given initially, the 48 hr PT cannot be used
- Must monitor for at least five d after last Vit K dose
- Anticoagulants
a. Refer if massive ingestion for INR (generally @ 48h)
