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Toxicology > Unit 1 - Toxic Gases > Flashcards

Unit 1 - Toxic Gases Flashcards

1
Q

What are the types of exposure that toxic gases can have?

A

Respiratory, dermal, and other

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2
Q

What local effects can toxic gases have?

A

Irritation, inflammation, edema, necrosis, fibrosis, and emphysema

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3
Q

What toxic gases are more common in large animal?

A

Nitrogen dioxide, hydrogen sulfide, ammonia, methane, carbon dioxide, and anhydrous

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4
Q

What toxic gases are more common in small animals?

A

carbon monoxide

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5
Q

What toxic gases are more common in avian species?

A

polytetrafluoroethylene

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6
Q

What is the most common gas in animal facilities?

A

ammonia (NH3)

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7
Q

What are the characteristics of ammonia?

A

colorless, lighter than air, and a shar pungent odor

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8
Q

Why is the ammonia odor worse in the winter months?

A

Because there is not a lot of air flow, it is very dry, and the areas are confined

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9
Q

What are the sources of ammonia?

A

Manure/slurry pits

Fertilizers

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10
Q

What clinical signs occur at 50 ppm of ammonia?

A

Decreased feed intake and decreased ciliary clearance

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11
Q

Why is decreased ciliary clearance bad?

A

It can increase the chance of respiratory disease because they are what work to get crap out of the lungs

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12
Q

What ocular clinical signs does ammonia cause?

A

Keratoconjunctivitis and lacrimation

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13
Q

What respiratory clinical signs does ammonia cause?

A

Increased nasal discharge, sneezing and coughing, pulmonary congestion, and dyspnea

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14
Q

What reproductive clinical signs does ammonia cause?

A

Decreased egg production

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15
Q

What terminal clinical signs are associated with ammonia?

A

Hypoxia, cyanosis, and violent seizures

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16
Q

What diagnostic tests are used to diagnose ammonia toxicosis?

A

There are really no reliable diagnostic tests - history of exposure and odor is all we’ve got

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17
Q

How is ammonia toxicosis treated?

A

Remove the source

Supportive care - eye ointment and abx

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18
Q

How is ammonia toxicosis prevented?

A

Provide adequate ventilation

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19
Q

What are the characteristics of anhydrous ammonia (Gas-NH3)?

A

Colorless (white vapor when spread), pungent odor, lighter than air, and water soluble

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20
Q

What are the sources of anhydrous ammonia?

A

Agricultural fertilizer, commercial refrigerant, and meth labs

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21
Q

What is the prime target for anhydrous ammonia?

A

mucous membranes

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22
Q

When anhydrous ammonia interacts with the water at the mucous membranes, what happens?

A

It creates ammonium hydroxide which is extremely caustic. This causes very strong alkali burns resulting in necrosis of the dermis, epithelium, and the muzzle

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23
Q

What clinical effects are associated with anhydrous ammonia?

A

Fluid accumulation in the lungs, respiratory distress
Sloughing of the respiratory tract epithelium
Corneal damage leading to blindness
Acute death

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24
Q

How is anhydrous ammonia toxicosis treated?

A

Supportive care, but the best option is euthanasia

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25
Q

How is anhydrous ammonia toxicosis prevented?

A

Ensure that equipment is functioning properly and DO NOT park anhydrous tanks near livestock or the house

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26
Q

What is the impact of anhydrous ammonia on human health?

A

It is extremely hazardous so you need to make sure that you have a self contained breathing apparatus and protective clothing

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27
Q

What should you do if you get exposed to anhydrous ammonia?

A

Remove your contaminated clothes and flush with water for 5 minutes

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28
Q

Why should you beware of the wind if there is an anhydrous ammonia leak, or a tank breaks, or something like that?

A

The gas could originally be blowing one way, but it can change direction and all of a sudden be blowing right in your face

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29
Q

What are the characteristics of carbon monoxide?

A

It is colorless, lighter than air, and odorless

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30
Q

What are the sources of carbon monoxide?

A

Inefficient combustion of carbon fuels in combination with inadequate ventilation

It can be acute or chronic

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31
Q

What can lead to inefficient combustion of carbon fuels?

A

Space heaters, grills, furnaces
Old/out of date heaters
Automobile exhaust
Fires

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32
Q

What can cause inadequate ventilation that leads to carbon monoxide poisoning?

A

Small space - farrowing room, chicken coop, and house garage
Clogged exhaust pipe/vent
Curtains that are ‘up’ in livestock facilities

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33
Q

What is the MOA of carbon monoxide?

A

CO binds to hemoglobin creating COHb. Oxygen cannot bind because CO is bound so there is less oxygen to the tissues causing anoxia

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34
Q

Fetal hemoglobin is more susceptible to CO. What clinical affects might you expect due to this?

A

Spontaneous abortions and still births

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35
Q

What acute clinical signs are associated with CO toxicity?

A

These are based on the degree of hypoxia: drowsiness, lethargy, incoordination, decreased heart excitability, cherry-red skin and mucous membranes
Dyspnea then coma then spasms then death
Abortions and stillbirths

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36
Q

What chronic clinical signs are associated with CO toxicosis?

A

Low exercise tolerance, abnormal posture, gait, and reflexes, and ECG abnormalities

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37
Q

What testing needs to be done ASAP in cases of suspected CO toxicosis?

A

Carboxyhemoglobin testing

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38
Q

What samples can be taken ante-mortem for carboxyhemoglobin testing? Post mortem?

A

ante-mortem - whole blood

Post-mortem - ‘lung juice’ and fetal thoracic fluid

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39
Q

What samples can be taken for histopath examination in CO cases?

A

the brain and the heart

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40
Q

COHb may return to normal after _______.

A

3-6 hours

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41
Q

What gross lesions are associated with CO toxicosis?

A

Bright cherry-red skin, blood, and mucous membranes

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42
Q

What microscopic lesions are associated with CO toxicosis?

A

Leukoencephalomalacia and myocardial necrosis

43
Q

What is the main goal of treatment for CO toxicosis?

A

Restore oxygen supply to the brain and heart

44
Q

How do we restore oxygen supply in cases of CO toxicosis?

A

Move patient to fresh air, maintain an airway, artificial respiration as needed, and possibly a hyperbaric chamber

45
Q

How is CO toxicosis prevented?

A

Maintain proper functioning of heaters and exhaust systems
Utilize CO detectors
Do not operate vehicles in enclosed spaces
Be vigilant if using combustible heating units indoors for livestock or other work

46
Q

Does CO toxicosis have a human health impact?

A

Yes - animals may be affected early, but humans are still susceptible

47
Q

What are the characteristics of CO2?

A

Colorless, heavier than air, and odorless

48
Q

What is the normal ppm of CO2 in the atmosphere?

Hint: The percent is 0.3%

A

3,000 ppm

49
Q

What are the sources of CO2 toxicosis?

A

Malfunctioning heaters, decomposing manure, and ill ventilated spaces

50
Q

T/F - CO2 is an asphixiant

A

True

51
Q

What are the clinical signs of CO2 toxicosis at 50,000 ppm?

A

Increased rate and depth of respiration

52
Q

What are the clinical signs of CO2 toxicosis at 100,000 ppm?

A

Distress

53
Q

What are the clinical signs of CO2 toxicosis at 400,000 ppm?

A

Staggering, coma, and death

54
Q

How is CO2 toxicosis diagnosed?

A

Testing - diagnosis by exclusion

Look at whole blood CO2 concentrations

55
Q

How is CO2 toxicosis treated?

A

fresh air

56
Q

What are the characteristics of hydrogen sulfide (H2S)?

A

It is colorless, heavier than air, and a ‘rotten egg’ smell

57
Q

What are the sources of hydrogen sulfide (H2S) toxicosis?

A

Decomposing manure and slurry pits, oil drilling, industrial sources, and high sulfur diets

58
Q

Toxicity due to H2S is common in what species?

A

livestock

59
Q

How is H2S gas produces?

A

H2S is formed by decomposition of sulfur contaminating acids
H2S bubbles are held in manure
H2S gas is released during manure agitation
H2S accumulates and rises to the level of animals

60
Q

What is the MOA of H2S?

A

Direct irritant to the eyes and lungs
CNS effects - inhibition of glutamate and serotonin
Metabolic effects - inhibition of cytochrome oxidase

61
Q

At ____ ppm H2S causes olfactory paralysis meaning you cannot smell the ‘rotten eggs.’

A

200 ppm

62
Q

At what concentration does H2S cause pulmonary edema and is potentially lethal?

A

> 500 ppm

63
Q

What clinical signs are associated with a ppm of >1000 H2S?

A

Respiratory paralysis, loss of consciousness, and collapse

64
Q

What clinical signs occur at >3000 ppm H2S?

A

Death (1-2 breaths)

65
Q

In what scenario can pumping of a manure pit lead to H2S toxicosis?

A

Electrical malfunction resulting in failure to drop curtains, turn on fans. or put up curtains and turn fans off
A humid day with no air movement could also be bad

66
Q

How can spatial H2S toxicosis occur?

A

Dead zones, location of agitator, and malfunction in 1 spot

67
Q

What lesions are associated with H2S toxicosis?

A

NON-SPECIFIC LESIONS
Edema of the lungs, brain, and intestines
Dark blood
H2S odor of tissues

68
Q

How is H2S toxicosis diagnosed?

A 
There are no reliable analytical tests:
Clinical signs of acute death
History of exposure and pumping pits
\+/- odor
Gas detectors
69
Q

What will histopath show in samples from a patient with H2S toxicosis?

A

Histopath will show neurodegeneration in thalamus and brain stem

70
Q

How is H2S toxicosis prevented?

A

Agitate and pump manure when animals are not present

IF they are around then ventilation is critical

71
Q

What can be done to improve ventilation in order to avoid H2S toxicosis?

A

Lower the curtains, ensure that the fans are running, double check that electronic controls are working, and perform on a windy/breezey

72
Q

What does elevated concentrations of H2S affect humans?

A

It gives them gas eye - which is similar to eye burn from a welder

73
Q

What does H2S do to humans at high concentrations?

A

1-2 breaths could lead to loss of consciousness and death

74
Q

T/F - If you notice someone is succombed to H2S, you should go in after them and get them out.

A

False - you gon’ die too

75
Q

What should you NOT do in regards to H2S?

A

Enter buildings that are actively being pumped
Attempt to retrieve items dropped into the pit
Attempt to rescue someone that has collapsed

76
Q

If you have to do one of the things on the ‘DO NOT’ list, what should you use?

A

A functioning SCBA must be used

77
Q

What can you DO in a H2S situation?

A 
Inform the producers of danger
Evaluate the environment
Adjust curtains (if safe to do so)
Post/adhere to warning signs
Allow ventilation following an incident
78
Q

What are the characteristics of methane gas?

A

It is colorless, lighter than air, and odorless

79
Q

What is the source of methane gase?

A

Manure and animal waste - you see bubbling pits

80
Q

Is there a human health hazard for methane?

A

Yes - it is an asphixiant at very high levels

81
Q

Why should you take caution around pits foaming?

A

Because they are explosive

82
Q

What are the characteristics of nitrogen dioxide?

A

Red-brown color, heavier than air, and pungent odor

83
Q

What are the sources of NO2?

A

Fermented grains and forages high in nitrate and laboratory settings

84
Q

What is the MOA of NO2?

A

It is a direct irritant that is extremely corrosive and causes lipid peroxidation

85
Q

What clinical signs are associated with NO2?

A

Upper airway irritation - coughing and choking as well as irritated an reddened mucous membranes
Delayed respiratory effects - tachycardia, pulmonary edema, dyspnea, and hypoxia

86
Q

NO2 toxicosis leads to chronic bronchitis and emphysema also known as what?

A

Silo fillers disease

87
Q

If the clinical signs of NO2 toxicosis progress rapidly, what can happen?

A

It may be fatal

88
Q

What lung lesions are associated with NO2 toxiocosis?

A

Edema, hyperemia and hemorrhage, emphysema, and bronchiolar inflammation

89
Q

What is diagnosis of NO2 toxicosis based on?

A

Clinical signs and history of exposure

90
Q

What is the human health impact of NO2?

A

It is an occupational health issue in agriculture that can cause chronic effects on the respiratory system

91
Q

How do you prevent NO2 toxicosis?

A

Protective gear, have a well ventilated area, and seal silage bags and silo doors

92
Q

What are the sources of polytetrafluoroethylene (PTFE)?

A

Non-stick cookware (teflon), shatter proof heat lamp bulbs, wiring, and ironing board covers

93
Q

What is the MOA of PTFE?

A

At greater than 280-530 C pyrolysis products form resulting in acidic volatile gas formation - this causes damage to alveoli

94
Q

What species does PTFE toxicosis affect?

A

Pet birds and poultry

95
Q

When is the onset of clinical signs of PTFE toxicosis?

A

Rapid

96
Q

What clinical effects does PFTE toxicosis cause?

A

Irritation - eye blinking
Anxiety - biting cage wire
Acute respiratory distress - tachypnea/dyspnea and audible respiration

97
Q

What samples should be taken for PFTE toxicosis diagnosis?

A

Fresh and fixed lung/air sacs

98
Q

Diagnosis of PFTE toxicosis is based on what?

A

History of exposure, post mortem lesions, and acute death (it is rapidly fatal)

99
Q

What gross lesions does PFTE toxicosis cause?

A

Pulmonary edema, congestion, and hemorrhage

100
Q

What microscopic lesions does PFTE toxicosis cause?

A

Severe necrotizing and hemorrhagic pneumonia +/- particles

101
Q

How is PFTE toxicosis treated?

A

Move them immediately to fresh air and provide supportive care (corticosteroids, abx, and fluids)

102
Q

How is PFTE toxicosis prevented?

A

Use non-stick cookware, remove pet birds from house/room, and double check the right equipment is being used in facilities

103
Q

What does PFTE cause in humans? Clinical signs?

A

Polymer Fume Fever - temporary, intense, flu-like syndrome

Toxicology (32 decks)

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