Pestcides

Question 1

Action of organophosphate and carbamate compounds

Answer 1

inhibit the enzyme cholinesterase

Question 2

Acetylcholinesterase (true or red blood cell acetylcholinesterase) is found primarily in________, ________, ____________.

Answer 2

erythrocyte membranes, nervous tissue, and skeletal muscle

Question 3

Inhibition of cholinesterase leads to_____________

Answer 3

acetylcholine accumulation at nerve synapses and neuromuscular junctions, resulting in overstimulation of acetylcholine receptors.

This initial overstimulation is followed by paralysis of cholinergic synaptic transmission in the CNS, in autonomic ganglia, at parasympathetic and some sympathetic nerve endings (e.g., sweat glands), and in somatic nerves.

Question 4

Excess acetylcholine results in a _________________ that manifests as a central and peripheral clinical toxidrome

Answer 4

cholinergic crisis

Question 5

Organophosphate compounds bind ____________ to acetylcholinesterase, thus inactivating the enzyme through the process of phosphorylation

Answer 5

irreversibly

Question 6

The term ________ describes the permanent, irreversible binding of the organophosphorus compound to the cholinesterase

Answer 6

aging

Question 7

Once aging occurs, the enzymatic activity of cholinesterase is____________ ______________, and new enzyme must be resynthesized over a period of weeks before clinical symptoms resolve and normal enzymatic function returns

Answer 7

permanently destroyed

Question 8

Antidotes are more effective if given ________ aging occurs

Answer 8

before

Question 9

Four clinical syndromes are described following organophosphate exposure:

Answer 9

AICO

acute poisoning
intermediate syndrome
chronic toxicity
organophosphate- induced delayed neuropathy

Question 10

acute organophosphate poisoning, most poisoned patients are symptomatic within the first _____hours and nearly all within the first _____ hours

Answer 10

8 hours

24 hours

Question 11

Acute organophosphate poisoning

Symptom onset is most rapid with ________

least rapid with ________

Answer 11

inhalation

transdermal absorption

Question 12

______________ is the presynaptic neurotransmitter at nicotinic receptors in the sympathetic ganglia and adrenal medulla

Answer 12

Acetylcholine

Question 13

Acetylcholine is the ______________neurotransmitter at ___________ receptors in the sympathetic ganglia and ____________

Answer 13

presynaptic

nicotinic

adrenal medulla

Question 14

in the sympathetic ganglia and adrenal medulla, inhibition of acetylcholinesterase at these locations results in sympathetic stimulation, producing ______, _______, _________, _________.

Answer 14

pallor, mydriasis, tachycardia, and hypertension

Question 15

Nicotinic stimulation at __________ __________ results in
________________, ___________, and _______________.

Answer 15

neuromuscular junctions

muscle fasciculations, cramps, and muscle weakness

Question 16

An intermediate syndrome occurring ________days after an organophosphate exposure is reported in up to 40% of patients following ingestion.

Answer 16

1 to 5 days

Question 17

In intermediate syndrome,

Clinical features include _____________________________________________________

Answer 17

paralysis of neck flexor muscles, muscles innervated by the cranial nerves, proximal limb muscles, and respiratory muscles (respiratory support may be needed)

Question 18

True or false

In intermediate syndrome, symptoms or signs of cholinergic excess are absent

Answer 18

True

Question 19

In intermediate syndrome, symptoms usually resolve within _____ days

Answer 19

7 days

Question 20

Chronic toxicity, seen primarily in agricultural workers with daily exposure, manifests as _________________

Answer 20

symmetrical sensorimotor axonopathy

This mixed sensorimotor syndrome may begin with leg cramps and progress to weakness and paralysis, mimicking features of the Guillain-Barré syndrome.

Question 21

This is characterized by cognitive dysfunction, impaired memory, mood changes, autonomic dysfunction, peripheral neuropathy, and extrapyramidal signs.

Answer 21

Organophosphate-induced delayed neuropathy OPDN

Question 22

The majority of patients severely poisoned with an organophosphorus insecticide will have the following symptoms:

Answer 22

altered mental status
pinpoint pupils
excessive sweating
difficulty breathing

Question 23

____________ and ___________ are both quantifiable but serve only as markers of cholinesterase activity at the synaptic junction.

Answer 23

Plasma butyrylcholinesterase

red cell acetylcholinesterase enzyme activity

Red cell acetylcholinesterase is a more accurate indicator of synaptic cholinesterase inhibition, but plasma butyrylcholinesterase is easier to assay and more available.

Question 24

Death occurs in untreated patients through a combination of __________, ____________, ____________.

Answer 24

bronchorrhea

respiratory muscle paralysis

CNS depression

Question 25

Immediate priorities following decontamination are

Answer 25

airway protection
provision of ventilation
reduction of bronchorrhea via adequate atropinization

reversal of respiratory muscle paralysis through administration of an oxime

Question 26

How to do decontamination?

Answer 26

All clothes and accessories must be removed completely, placed in plastic bags, and disposed of as hazardous materials.

The patient should be immediately decontaminated externally with copious amounts of a mild detergent such as dishwashing liquid and water.

Decontamination includes the scalp, hair, fingernails, skin, conjunctivae, and skin folds.

Body fluids should be treated as contaminated.

Abrasion or irritation of the skin should be avoided.

Contaminated runoff water should be contained and disposed of as hazardous material.

Instruments used can be decontaminated using chlorine bleach.

Question 27

Acute exposure monitoring and airway

Answer 27

Patients with acute exposures should be placed on oxygen, a cardiac monitor, and pulse oximeter.

A 100% nonrebreather mask will optimize oxygenation

Question 28

This kind of agent should be used when neuromuscular blockade is needed

Answer 28

nondepolarizing

Question 29

True or false

Succinylcholine is metabolized by plasma butyrylcholinesterase; therefore, prolonged paralysis may result.

Answer 29

True

Question 30

This is the antidote for significant organophosphate poisonings

Answer 30

Atropine

Question 31

Action of atropine

Answer 31

As a competitive antagonist of acetylcholine at central and peripheral muscarinic receptors, atropine will reverse the effects secondary to excessive cholinergic stimulation.

Question 32

Dose of atropine

Answer 32

initial dose of 1.2 to 3.0 milligrams

is given depending on severity of symptoms.

The dose is doubled every 5 minutes until the following are achieved: chest clear on auscultation, heart rate >80 beats/min, and systolic blood pressure >80 mm Hg.

Question 33

Therapeutic End points in atropine administration

Answer 33

chest clear on auscultation

heart rate >80 beats/min

systolic blood pressure >80 mm Hg

Question 34

True or false

Pupillary dilatation is not a therapeutic end point

Answer 34

True

Question 35

True or false

Tachycardia is not a contraindication to the use of atropine in organophosphorus poisoning because tachycardia can occur secondary to bronchospasm or bronchorrhea with hypoxia, which can be reversed with atropine.

Answer 35

True

Question 36

True or false

atropine reduces respiratory tract secretions but does not reverse muscle weakness

Answer 36

True

Question 37

T or F

Atropine may prevent or abort seizures (due to cholinergic overstimulation) that occur within the first few minutes of exposure.

Answer 37

True

Question 38

Minimal exposures may require only decontamination and ________hours of observation in the ED to detect delayed effects.

Answer 38

6 to 8 hours

Question 39

Reexposure should be avoided because

Answer 39

sequential exposures can result in cumulative toxicity

Question 40

In significant poisonings, the end point of therapy is determined by

Answer 40

absence of signs and symptoms on withholding of pralidoxime

Question 41

Most patients respond to pralidoxime therapy with an increase in acetylcholinesterase levels within_______

Answer 41

48 hours

Question 42

If there is no post-hypoxic brain damage and if the patient is treated early, symptomatic recovery occurs in ____________

Answer 42

10 days

Question 43

Action of pralidoxime

Answer 43

displace organophosphates from the active site of acetylcholinesterase, thus reactivating the enzyme

reverses muscle paralysis if given early, before aging occurs

It ameliorates muscarinic, nicotinic, and CNS symptoms

Question 44

Action of Carbamates

Answer 44

transiently and reversibly bind to and inhibit the cholinesterase enzyme.

Question 45

major difference from organophosphate poisoning, in carbamate poisoning

Answer 45

Regeneration of enzyme activity by dissociation of the carbamate–cholinesterase bond occurs within minutes to a few hours and involves rapid, spontaneous hydrolysis of the carbamate–cholinesterase bond. Therefore, aging does not occur, and restoration of normal function does not require generation of new enzyme.