Toxicology-Cont'd-2

Front 1

What the locomotor manifestations from chlorinated hydrocarbon toxicity?

Back 1

fasiculations, spasms, seizures

Front 2

What autonomic phenomena are manifested with chlorinated hydrocarbon toxicity?

Back 2

emesis and salivation

Front 3

What dependent signs can be seen with chlorinated hydrocarbon toxicity?

Back 3

increase body temperature, increase respiratory rate, and increase depth of respiration

Front 4

How can toxicity be increased?

Back 4

by fasting or stress which mobilizes fat stores and release of chemical residues

Front 5

What structures are most significant for a tissue residue analysis?

Back 5

brain and liver residues

Front 6

What characteristic lesions can seen in toxicity

Back 6

none, pulmonary congestion and edema, and hemorrhages in the GI tract

Front 7

What treatment is used for skin toxicity?

Back 7

bathe

Front 8

What treatment is used for GI toxicity?

Back 8

induce emesis, activated charcoal, cathartic

Front 9

What treatment is used for CNS toxicity?

Back 9

control seizure activity with benzodiazepine(diazepam) and barbiturate(phenobarbital)

Front 10

What drug may enhance elimination of toxin?

Back 10

phenobarbital

Front 11

What is the environmental concern in raptors?

Back 11

eggshell thinning cause estrogenic effects in birds leading to infertility

Front 12

What are the insecticides of natural origin?

Back 12

pyrethrins, pyrethroids, nicotene, rotenone

Front 13

Which plant is a major source of pyrethrum?

Back 13

chrysanthemums

Front 14

What are the pyrethrins?

Back 14

Pyrethrin I and II, Cinerin I and II, and Jasmolin I and II

Front 15

What are the synthetic pyrethrins less toxic to non insect spp?

Back 15

pyrethroids

Front 16

Which pyrethroids contain CN moiety

Back 16

the cyano group

Front 17

What is the presence of CN in type I pyrethroid and type II?

Back 17

type I- absent, type II- present

Front 18

Which of the natural origin insectides have the highest environmental staability and why?

Back 18

pyrethroids, because the pyrethrings are light sensitive and degrade in air

Front 19

Why are pyrethrins less environmentally stable than pyrethroids?

Back 19

because pyrethrins are light sensitive and degrade in air

Front 20

What means of administration has the highest toxic effect?

Back 20

parenteral administration

Front 21

Which spp. is pyrethrins and pyrethroids most and least toxic to?

Back 21

most toxic to insects and fish, least toxic to mammals and birds

Front 22

What spp. are pyrethrins and pyrethroids best absorbed?

Back 22

mammals and birds

Front 23

What absorption is the least, and what is moderate for pyrethroids and pyrethrins?

Back 23

moderate absorption in the GI(broken down in GI too!)
low dermal absorption

Front 24

What is the distribution of pyrethrins and pyrethroids?

Back 24

distribution throughout the body including the CNS

Front 25

What is the metabolism of pyrethrins and pyrethroids?

Back 25

metabolism is very rapid

Front 26

What enzymes aid in pyrethrin and pyrethroid metabolism?

Back 26

plasma esterases and hepatic oxidases

Front 27

Is the Cis isomer of pyrethrins and pyrethroids more or less toxic? Do they degrade faster or slower?

Back 27

Cis isomer degrade slower and they are more toxic

Front 28

What is the MOA of pyrethrins and pyrethroids?

Back 28

1. CNS Stimulant- affects Na channels in membranes, suppress inward flow of Na and outward flow of K
2. inhibit ATPase activity
3. II- interferes with receptor binding of GABA and glutamic acid

Front 29

Which pyrethroid is most toxic?

Back 29

Pyrethroid II

Front 30

What clinical signs can be seen with pyrethrin/pyrethroid intoxication?

Back 30

1. aggressive behavior
2. increase sensitivity to external stimuli
3. tremors
4. prostration
5. increase body temperature
6. chewing movements
7. profuse salivation
8. body tremors and writhing
9. seizures

Front 31

What clinical signs can be seen with severe intoxication of pyrethrins/pyrthroids?

Back 31

respiratory collapse
cardiovascular collapse

Front 32

What is the most important information when diagnosis of intoxication of pyrethrins/pyrethroids?

Back 32

all information is based on the laboratory experience

Front 33

How do you treat dermal exposure to pyrethrins/pyrethroids?

Back 33

bathe

Front 34

How do you treat oral exposure to pyrethrins/pyrethroids?

Back 34

emetic, activated charcoal, cathartic

Front 35

How do you counteract CNS effects of pyrethrins/pyrethroids intoxication?

Back 35

benzodiazepines(diazepam) and barbituates(phenobarbital)

Front 36

What natural originated insecticide is significantly toxic to all animals?

Back 36

nicotine

Front 37

What is the MOA of nicotine?

Back 37

acts at all nicotinic cholinergic receptors (CNS, ANS ganglia, skeletal neuromuscular junction, mimics ACh)

Front 38

What is absorption of nicotine?

Back 38

rapid absorption across all mucosal surfaces, across skin, and BBB. There is also absorption via GI tract, and Respiratory tract

Front 39

Is nicotine lipophillic or lipophobic?

Back 39

lipophilic

Front 40

What are the initial effects of nicotine toxicity?

Back 40

salivation
diarrhea
muscle tremors
excitation
increased respiration rate

Front 41

What are the second effects of nicotine toxicity?

Back 41

skeletal muscle weakness
ANS- Bradycardia
CNS- Depression and coma, decreased respiratory rate

Front 42

Is there lethality with nicotine toxicity?

Back 42

yes, due to repiratory failure and/or cardiac arrest

Front 43

What is the treatment for nicotine toxicity?

Back 43

if dermal- wash, if oral-gastric lavage, also administer artificial respiration and stimulants such as caffeine