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Tox Final Exam > Toxic Gases > Flashcards

Toxic Gases Flashcards

1
Q

List the toxic gases covered in this course!

A

ammonia, hydrogen sulfide, carbon monoxide, nitrogen oxide gases and sulfur oxide gases

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2
Q

Source of ammonia (NH3)?

A

decomposing manure in confined animal houses, burning nylon/plastics, anhydrous NH3 used in agriculture fertilizer

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3
Q

Properties of ammonia?

A

sharp odor, heavier than air, soluble in water and readily reacts with hydroxyl ions in moist mucous membranes to form ammonium hydroxide–irritant and caustic

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4
Q

Humans can detect about ____ ppm ammonia in air and their eyes burn at _____ ppm.

A

10; 25-35 ppm

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5
Q

Ammonia is most frequently found in high concentrations where?

A

animal houses–can reach 50 ppm

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6
Q

What species are most susceptible to ammonia gas toxicity?

A

livestock–swine, poultry

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7
Q

ADME of ammonia?

A

A=inhalation
D=to tissue cells
NH3 converted to strong irritant on MM

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8
Q

Exposure to _______ ppm can cause acute death.

A

5,000

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9
Q

MOA of ammonia toxicosis?

A

direct irritation of MM, increased susceptibility to resp infection, decreased growth in young, pulmonary edema and lung congestion, alkalosis and compensatory acidosis, inhibit TCA cycle

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10
Q

Cause of death d/t ammonia toxicosis?

A

asphyxia and partly d/t electrolyte and cellular metabolic effects

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11
Q

Clinical signs for ammonia toxicosis?

A

red MM, lacrimation, coughing, sneezing, nasal discharge, keeping eyes shut, decreased growth rate, decreased egg production, dyspnea
terminal signs: cyanosis, CNS stimulation, clonic convulsions

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12
Q

Lab diagnosis for ammonia toxicosis?

A

chem analysis not routinely made w/ toxic gases

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13
Q

Differential diagnosis for ammonia toxicosis?

A

dzs that cause resp insufficiency–> inhaled irritants (hydrogen sulfide, nitrogen, oxides, sulfur oxides, fumes, dusts, vapors), organophosphates, polychlorinated biphenyls, cardiac glycosides

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14
Q

Treatment for ammonia toxicosis?

A

remove source of NH3, animal premises kept clean and well ventilated, fresh air for dyspnea, soothing ointments applied to the eyes and ABs to prevent secondary infections, diuretics for pulmonary edema, tx secondary infections (pneumonia)

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15
Q

Source of hydrogen sulfide (H2S)?

A

decomposition of urine/feces in underfloor waste pits, deep litter, manure packs, sewage and other organic matter containing sulfur. by-product or waste material from industry. may be liberated in coal pits, gas wells or sulfur springs.

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16
Q

Name some gases liberated from the decomposition of urine and feces?

A

hydrogen sulfide, ammonia, carbon dioxide and methane

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17
Q

Properties of hydrogen sulfide?

A

colorless, odor of rotten eggs, heavier than air, irritant (converted to sulfuric acid in solution and forms sodium sulfide on contact w/ moist MM)

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18
Q

Hydrogen sulfide reacts with what in the GIT and maybe tissues to form black or dark-colored compounds?

A

silver, iron, lead and other metals

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19
Q

T/F Hydrogen sulfide is the second most dangerous sewage gas.

A

FALSE! It is the most dangerous!

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20
Q

Humans can detect hydrogen sulfide in air at ______ ppm.

A

0.025 ppm

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21
Q

Symptoms at different ppms of hydrogen sulfide.

A

20 ppm–> ocular irritation
50 ppm–> severe symptoms
200 ppm–> olfactory accommodation (Danger!)
400 ppm–> sudden exposure can be quickly fatal
1000 ppm–> rapid unconsciousness and death in 1 hr

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22
Q

T/F Acute hydrogen sulfide poisoning is directly responsible for more deaths in closed animal facilities than any other gases.

A

TRUE

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23
Q

ADME of hydrogen sulfide?

A

A=lungs and GIT
M=converted to alkali sulfides in blood, some sulfide trapped by natural disulfides such as glutathione in blood
E=feces as iron sulfide and urine as sulfate

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24
Q

MOA of hydrogen sulfide toxicosis?

A

direct irritation of MM, inhibition of cellular respiration by inhibiting cytochrome oxidate–can lead to permanent effects on NS, stimulation of chemoreceptors of the carotid body interfering with respiratory drive

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25
Q

What are the effects of stimulating the chemoreceptors of the carotid body?

A

causes hyperpnea–depletion of CO2–apnea–either recover or die from asphyxiation

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26
Q

Clinical signs of larger concentrations of hydrogen sulfide?

A

sudden collapse, cyanosis, dyspnea, anoxic convulsions and rapid death

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27
Q

Clinical signs of smaller concentrations of hydrogen sulfide?

A

signs of irritation to ocular, respiratory mucosa and lungs (like ammonia)

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28
Q

Lesions seen with hydrogen sulfide toxicosis?

A

blood is dark and may not clot, tissues may be dark or greenish purple, carcass may have the odor of hydrogen sulfide (sewage), if ingested the GI contents may be black or dark gray w/ sewage odor

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29
Q

Differential diagnosis for hydrogen sulfide toxicosis?

A

Same as ammonia

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30
Q

Treatment for hydrogen sulfide toxicosis?

A

remove source, sodium nitrite IV, hydrated sulfide anion, oxygen therapy, ventilation, supportive tx

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31
Q

What is the MOA of sodium nitrite IV?

A

forming methemoglobin that binds the hydrated sulfide radical and reactivate cytochrome oxidase

32
Q

What is the MOA of hydrated sulfide anion?

A

can interact w/ disulfides such as oxidized glutathione

33
Q

Extra information regarding hydrogen sulfide toxicosis.

A

monitor animals when agitation of pit started. if clinical signs shut off pump. do not rescue animals immediately (risk for human exposure).

34
Q

Source of carbon monoxide?

A

fires, propane powered equipment–space heaters, portable cookers, driveway de-icers, automobile exhaust in confined spaces

35
Q

Properties of carbon monoxide?

A

odorless and colorless

36
Q

T/F Carbon monoxide poisoning is very common in pets.

A

FALSE–not common

37
Q

What species will you occasionally see carbon monoxide poisoning?

A

dog, cat, livestock or chickens

38
Q

T/F Smaller animals have faster breathing rates and smaller Vd (volume of distribution) so may show toxicity before humans.

A

TRUE–Canary in a coal mine!

39
Q

Carbon monoxide greater than ______ ppm can cause clinical signs and death within 1 hr.

A

1000 ppm

40
Q

T/F Fetuses are not affected by carbon monoxide poisoning.

A

FALSE–they are actually more sensitive!

41
Q

MOA of carbon monoxide poisoning?

A

combines with hemoglobin to form carboxyhemoglobin which cannot carry oxygen, carboxyhemoglobin interferes w/ release of oxygen carried by normal hemoglobin, competes w/ O2 for binding sites on myoglobin which is worsened in hypoxia, some interference w/ cellular respiration at the mitochondrial level (can lead to free radical formation and attraction of leukocytes)

42
Q

What is the cause of death from carbon monoxide toxicosis?

A

hypoxia–death at 60-70% COHb (breathing 13% CO for 1 hr=death)

43
Q

Hemoglobin affinity for CO is ____ times greater than for O2.

A

240 times!!

44
Q

Clinical signs of carbon monoxide toxicosis?

A

sudden death, hypoxia, drowsiness, incoordination, dyspnea, lethargy, coma, stillborn fetuses in swine and sheep

45
Q

Lesions seen in carbon monoxide toxicosis?

A

bright red blood, MM are healthy pink, no significant lesions in acute cases, chronic cases may see brain edema, hemorrhage and necrosis

46
Q

T/F Chonic cases of carbon monoxide poisoning can cause deafness in dogs and cats.

A

TRUE!!!

47
Q

Laboratory diagnosis for carbon monoxide?

A

measuring CO in air, percentage of carboxyhemoglobin in blood

48
Q

Treatment for carbon monoxide toxicosis?

A

oxygen or 5% CO2 in oxygen w/ positive pressure–>oxygen displaces CO and CO2 induces hypernea, blood transfusion, fluids for acidosis (bicarb use is controversial)
note: recovery may not happen

49
Q

Why is bicarbonate use in treating carbon monoxide toxicosis controversial?

A

may affect O2 dissociation curve

50
Q

Name the 2 different nitrogen oxide gases?

A

nitrogen dioxide (NO2) and nitrogen tetraoxide (N2O4)

51
Q

Source of nitrogen oxide gases?

A

produced by incomplete reduction of nitrates during fermentation process in silos

52
Q

What is the nickname for nitrogen oxide toxicosis in people?

A

silo filler’s disease

53
Q

Properties of nitrogen oxide?

A

nitrogen dioxide gas is reddish brown and nitrogen tetraoxide has is colorless, mixture of the 2 is yellow or yellow-brown

54
Q

BORING nitrogen oxide gas notes….

A
  • -NO2 is heavier than air but the gases are about as dense as air – forms layers on top of silage and settles down the shute
  • -In water, the gases form nitric acid (HNO3) and nitric oxide (NO)
  • -Alkali converts the gases to nitrates and nitrites
  • -The gas mixture has an irritating chlorine-like odor
  • -In smogs sunlight converts NO and oxygen to NO2 and ozone
  • -Ozone may contribute to smog-induced lung damage (emphysema)
55
Q

Humans can smell ____ ppm of nitrogen oxide gas.

A

1-3

56
Q

T/F Brief exposure to high concentrations is more toxic than chronic exposure to low concentrations of nitrogen oxide gas.

A

TRUE

57
Q

Long exposure to a few ppm of nitrogen oxide gas can increase risk for _________.

A

respiratory infections

58
Q

_______ ppm causes mild to moderate irritation of eyes and upper airway resp mucosa.

A

50-150

59
Q

Nitrogen dioxide and tetraoxide gases form ______ upon contact with MM.

A

nitric acid

60
Q

Absorption of nitrogen oxide gas?

A

both nitric acid and the gases cross resp mucosa–cause cell damage

61
Q

Prevention of nitrogen oxide toxicosis?

A

do not enter animal quarters that develop the irritant odor or yellow haze in the air

62
Q

MOA of nitrogen oxide toxicosis?

A

direct irritation of MM by nitric acid, lung damage (due to rxn w/ polyunsaturated fatty acids of lung cellular lipids)

63
Q

T/F Because of nitric acid’s high solubility in water it can pass through upper resp tract and cause lung damage.

A

FALSE–low solubility in water!

64
Q

Cause of death from nitrogen oxide toxicosis?

A

hypoxia

65
Q

Clinical signs of nitrogen oxide toxicosis?

A

resp signs–>similar to ammonia poisoning

66
Q

Lesions seen in nitrogen oxide toxicosis?

A

pulmonary edema, hemorrhage, emphysema, and inflamm of bronchioles which may contain granulation tissues–cyanosis, methemoglobinemia and necrosis of skeletal muscles

67
Q

Treatment of nitrogen oxide toxicosis?

A

supportive treatment–>fresh air, oxygen, diuretics (pulmonary edema), and antioxidants such as NAC and VitE–methylene blue IV for methemoglobinemia

68
Q

Prognosis of nitrogen oxide toxicosis?

A

poor in animals exposed to large concentrations

69
Q

Name the 2 different sulfur oxide gases.

A

sulfur dioxide (SO2) and sulfur trioxide (SO3)

70
Q

Source of the sulfur oxide gases?

A

industrial pollutants

71
Q

Sulfur oxide gases are sharply irritant to MM because?

A

bc the gases form sulfurous and sulfuric acids on contact w/ water

72
Q

The odor of sulfur oxide causes what symptoms?

A

coughing, choking and suffocation

73
Q

Sulfur dioxide gas toxicity at different ppms.

A

500 ppm–30-60 minutes fatal to cats
500 ppm–1 hr dangerous to grazing animals
5-40 ppm–8 days causes poisoning in pigs

74
Q

MOA of sulfur oxide gas toxiosis?

A

direct irritation of MM, reflex bronchoconstriction, lung damage

75
Q

Cause of death d/t sulfur oxide gas toxicosis?

A

hypoxia

76
Q

T/F Clinical signs, lesions, diagnosis and treatment are similar to other toxic gases.

A

TRUE

Tox Final Exam (9 decks)

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