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Flashcards in Toxic Gases Deck (69):
1

Ammonia chemical compound

NH3

2

Sources of ammonia

- decomposing manure
- burning nylon and plastic
- fertilizers

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properties of ammonia

- sharp odor
- heavier than air
- soluble in water
- readily reacts with moisture in mucous membranes

4

ammonia toxicity

- most frequently found in high concentrations in animal houses
- livestock are most susceptible

5

Ppm level of ammonia that causes acute death

5,000

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ammonia toxicokinetics

- strong irritant on mucous membranes
- absorbed by inhalation

7

ammonia MOA

- continuous irritation causes respiratory infections, pulmonary edema and lung congestion
- decreased growth in young animals
- alkalosis and compensatory acidosis
- inhibits TCA cycle

8

Death from ammonia is due to

asphyxia and electrolyte/cellular metabolic effects

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Clinical signs of ammonia toxicity

- red mucous membranes, crying, sneezing, nasal discharge
- fluid in lungs
- cyanosis, CNS stimulation and clonic convulsions

10

CS of ammonia toxicity in birds

decreased growth rate and egg production

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treatment of ammonia toxicity

- remove source
- fresh air
- soothing ointment for eyes
- diuretics for pulmonary edema
- treat secondary infections

12

hydrogen sulfide chemical formula

H2S

13

sources of hydrogen sulfide

- liberated from the decomposition of urine and feces in underfloor waste pits, deep litter, sewage, etc.
- stuff to do with poop

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toxicity of hydrogen sulfide

- most dangerous sewage gas
- humans die at 1000 ppm

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Acute toxic levels of hydrogen sulfide in mammals

500-800 ppm

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hydrogen sulfide toxicokinetics

- easily absorbed in lungs and GI
- converted to alkali sulfides in blood
- can get trapped as glutathione
- excreted in feces

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MOA of hydrogen sulfide

- irritation of mucous membranes
- inhibits cellular respiration
- interferes with chemoreceptors --> hyperpnea

18

CS of hydrogen sulfide poisoning

- collapse, cyanosis, dyspnea, anoxic convulsions, death
- lower conc. = irritation of eyes and lungs

19

Lesions with hydrogen sulfide poisoning

- blood is dark and may not clot
- tissue can be dark or green/ purple
- carcass might smell like sewage
- Gi contents may be black or dark gray

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Properties of hydrogen sulfide

- colorless
- odor of rotten eggs
- heavier than air
- flammable
- reacts with other metals to make the dark compound

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treatment of hydrogen sulfide poisoning

- removal of source (duh)
- sodium nitrate IV
- oxygen therapy, ventilation and supportive stuff

22

What is flatus

gas in the stomach

23

Carbon monoxide chemical formula

CO

24

Sources of exposure to carbon monoxide

- incomplete combustion of carbon products (wood, paper, etc)
- propane powered equipment
- car exhaust in confined spaces

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Properties of carbon monoxide

- odorless and colorless

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Toxicity with carbon monoxide is common or uncommon

- uncommon
- canaries used in coal mines
- fetus is more sensitive

27

Ppm at which clinical signs and death appear from carbon monoxide poisoning

- 1,000
- occurs within one hour

28

MOA of carbon monoxide

- CO combines with hemoglobin to form carboxyhemoglobin
- cannot carry oxygen
- interferes with release of oxygen carried by normal hemoglobin

29

Is hemoglobin more attracted to oxygen or CO

- CO
- 240X greater affinity

30

What is it called when carboxyhemoglobin interferes with the release of oxygen

- Haldane Effect
- Leftward shift of O2 dissociation curve

31

MOA of carbon monoxide

- Death from hypoxia
- can interfere with cellular respiration in the mitochondria

32

Clinical signs of carbon monoxide poisoning

- sudden death
- low dose= hypoxia, drowsiness, incoordination, dyspnea, lethargy, coma
- death at 60-70% CO in one hour

33

CO concentrations greater than 250 ppm cause

- increased number of stillborn fetuses in pigs and sheep

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Lesions with carbon monoxide poisoning

- bright red blood
- healthy pink mucosa
- chronic= brain edema, hemorrhage, and necrosis

35

Lab work results

- measure CO in air
- measure carboxyhemoglobin in blood (correlation not great)

36

Treatment of carbon monoxide

- oxygen or 5% CO2 in mask/ tube/ chamber with positive pressure
- Blood transfusion

37

Nitrogen oxide poisoning is also called

Silo filler's disease

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Nitrogen oxide gases are produced....

by incomplete reduction of nitrates during fermentation in silos

39

NO2 gas properties

- reddish brown
- heavier than air
- forms layers on top of silage and then settles down the chute

40

N2O4 properties

- colorless

41

NO2 and N2O4 mixed together

yellow or yellow-brown

42

Nitrogen oxide gases smell like

chlorine-like when mixed

43

Sunlight and nitrogen oxide gases

creates NO2 and ozone (O3)

44

Nitrogen oxide gas toxicity

- 50-150 ppm causes mild irritation to eyes and upper respiratory
- Swine die from 250-310 ppm

45

What is the worst way to be exposed to nitrogen oxide gases? (acute/ chronic) (high vs. low conc)

acute and high

46

Nitrogen oxide gas toxicokinetics

- will see yellow haze in the air
- form nitric acid when it contacts mucous membranes

47

MOA of nitrogen oxide gases

- direct irritation of membranes
- pass through upper respiratory tract and cause lung damage
- death from hypoxia

48

Nitrogen oxide gas CS

respiratory signs

49

Lesions with nitrogen oxide gases

- pulmonary edema, hemorrhage, emphysema and inflammation of bronchioles
- cyanosis, methemoglobinemia and necrosis of skeletal muscles

50

What is methemoglobin

A form of hemoglobin where ferric iron has a lower binding affinity for oxygen than ferrous iron

51

Treatments of nitrogen oxide gases

- supportive treatment (fresh air, oxygen, diuretics)
- ointments

52

Prognosis for nitrogen oxide gases

- poor in animals acute/ high conc.
- good with chronic at low conc.

53

Sulfur oxide gas source

- industrial pollutants
- fossil fuel combustion at power plants and industrial facilities

54

Sulfur oxide gas properties

- sharp irritant to membranes
- causes coughing, choking and suffocation

55

sulfur oxide toxicity

- 500 ppm= fatal in cats within 30-60 min, dangerous to grazing animals
- 5-40 ppm over 8 days causes poisoning in pigs

56

MOA of sulfur oxide gases

- direct irritation of mucosa
- reflex bronchoconstriction
- lung damage
- death by hypoxia

57

Clinical signs of sulfur oxide

- respiratory and irritation
- treatment is similar to other gases

58

smoke inhalation

- 80% of fire related deaths
- synthetic materials are more flame retardant but more toxic if they do burn

59

Smoke toxicity

- younger pets are more likely to recover
- no one typical kind of smoke
- super heated air causes thermal burns
- burns increase toxicity

60

MOA of smoke inhalation

- simple asphyxiants by displacing oxygen in the air (CO2 and methane)
- chemical asphyxiants preventing the uptake of oxygen (CO)
- irritants

61

Clinical signs of smoke inhalation

- respiratory (cough, wheezing, rales, crackles, etc.)
- cardiovascular (tachycardia, hypoxemia, hypotension, arrhythmias)
- Irritation of membranes
- CNS signs

62

Treatment of smoke inhalation

- oxygen support and removal from environment
- Beta 2 agonists
- No steroids
- no cough suppressants

63

Indications for intubation in smoke inhalation patient

- SpO2 less than 90% with oxygen
- respiratory depression or edema
- facial burns

64

how long should you monitor a smoke inhalation patient

- 6-8 hours post exposure
- recheck in 72 hours

65

High water soluble smoke inhalation irritants

- aldehyde
- sulfur dioxide
- ammonia
- hydrogen chloride

66

Intermediate water soluble smoke inhalation irritants

- chlorine
- isocyanates

67

Poor water soluble smoke inhalation irritants

- Phosgene
- Nitrogen oxides

68

What is soot

- carbon particles suspended in gas and hot air
- binds to mucosa, allowing other irritants to also bind
- sulfur dioxide especially!!!

69

The more soluble the toxin

the greater the injury to the mucosa