33 - Toxic Gases Flashcards
1
Q
Toxic gases in general and vet med
A
- relative toxicity is highly variable ranging from irritation, suffocation to inhibition of cellular respiration
- *Ventilation is an important factor in many instances.
2
Q
Ammonia (NH3)
A
- may be generated from sewage pits or fertilizers
- *Poor ventilation in intensive animal or poultry facilities is often an important factor
- a strong base and is highly irritating and caustic
3
Q
Ammonia (NH3) actue exposure will produce
A
- coughing
- sneezing
- dyspnea (pulmonary edema)
- lacrimation
4
Q
Ammonia (NH3): treatment
A
- improve ventilation
5
Q
What 2 gases are frequently formed in silos that are associated with incomplete reduction of nitrate ion?
A
- NO2 and N2O4
o produce silofillers disease in man and ultimately cause bronchiolitis obliterans
o highly toxic
o Following exposure, the water in the moist membranes of the lung tissue reacts with NO2 to nitric acid - (Nitrous oxide (laughing gas) is N2O and should not be confused with the toxic gases)
6
Q
What do the caustic properties of nitric acid cause?
A
- Irritation
- Pulmonary edema
- Direct alveolar membrane damage
- Methemoglobin is also produced, but it is a poor indicator of toxicity
7
Q
Nitrogen Oxide Gases: Clinical manifestations
A
- dyspnea
- coughing
- salivation, lacrimation
- reddened mucous membranes
- bronchitis, emphysema
- Secondary bacterial pneumonia associated with impaired ciliary action and clearance mechanisms may be observed.
8
Q
Nitrogen Oxide Gases: prognosis
A
- Poor
9
Q
Nitrogen Oxide Gases: treatment
A
- improve ventilation
10
Q
Nitrogen Oxide Gases: DDx
A
- ANTU
- Nitrite
- Organophosphate/carbamate insecticides
- Cyanide
- Urea
11
Q
Sulfur Oxide Gases
A
- including sulfur dioxide (SO2) and sulfur trioxide (SO3)
- Produced primarily from industrial sources including high sulfur coal or oil combustion
- Component of smog and acid rain
12
Q
What might forage contamination with sulfur oxide gas compounds contribute to?
A
- Mineral imbalances resulting in selenium or copper deficiency
o In western Canada, the oil industry has been a major contributor to this problem
13
Q
Sulfur Oxide Gases: mechanism of action
A
- Similar to the nitrogen oxide gases
- sulfur oxide gases react with water in the lungs to form sulfuric acid
- *caustic action of the acid results in irritation, pulmonary edema, hemorrhage and emphysema
14
Q
Sulfur Oxide Gases: clinical manifestations
A
- lacrimation, salivation
- coughing
- broncoconstriction
- cyanosis
- red mucous membranes
15
Q
Sulfur Oxide Gases: Pathology
A
- pulmonary edema
- emphysema
- atelectasis
- hemorrhage
- fibrosis (chronic)
- secondary bacterial pneumonia
16
Q
Sulfur Oxide Gases: treatment
A
- Remove from the contaminated area.
17
Q
Sulfur Oxide Gases: prognosis
A
- poor if high-level exposure occurs
18
Q
Hydrogen Sulfide (H2S)
A
- primary sources: Flare gas emissions and sewage pits
- Extremely toxic
o Acute deaths in animals and workers usually result - Blocked or non-functional sewage pits are most frequently involved.
19
Q
Sewage pits produce four major gases: what are they?
A
- hydrogen sulfide: highly toxic
- ammonia: toxic
- carbon dioxide: relatively non-toxic
- methane: relatively non-toxic, but explosive
20
Q
Hydrogen Sulfide (H2S): mechanism of action
A
- Single breath may be fatal=MUST WEAR PROPER SAFETY EQUIPMENT
21
Q
Hydrogen Sulfide (H2S): effects
A
- Irritation: H2S reacts with sodium to form Na2S=produce pulmonary edema
- Hypoxia: H2S forms disulfide bonds with the cytochrome oxidase enzyme. (ETC affected: similar to cyanide)Cellular respiration stops and tissue anoxia occurs rapidly.
- Sulfhemoglobin: hydrogen sulfide also bonds to hemoglobin causing inactivation
**3 things result in severe and rapid clinical manifestations and most frequently death
22
Q
Hydrogen Sulfide (H2S): Clinical manifestations
A
- If inhaled, the gas rapidly destroys the sense of smell
o A false sense of security is perceived as the smell disappears - coughing
- lacrimation
- pulmonary edema, dyspnea
- bronchoconstriction
- cyanosis
- anoxic terminal convulsions
23
Q
Hydrogen Sulfide (H2S): pathology
A
- Few gross lesions may be present
o May be a smell of hydrogen sulfide in the tissues
24
Q
Hydrogen Sulfide (H2S): treatment
A
- ventilation, oxygen
- usually fatal
25
Hydrogen Sulfide (H2S): diagnosis
- Usually circumstantial evidence suggests sewage pit or flare gas involvement
- Dyspnea and sudden death are often key features.
26
Hydrogen Sulfide (H2S): DDx
1) ANTU
2) ammonia
3) sulfur oxide gases
4) organophosphate/carbamate insecticides
5) organochlorine insecticides
6) nitrite
7) cyanide
27
Carbon Monoxide (CO)
- often associated with poor ventilation
- Car exhaust or improper furnace function are frequent causes
28
CO: mechanism of action
- small molecule=rapidly absorbed
- reacts quickly with hemoglobin to form carboxyhemoglobin
- NOT a cumulative poison
o It is in equilibrium with oxygen as it completes for hemoglobin
- CO has about a 200 fold great affinity for hemoglobin.
29
CO: Clinical manifestations
- considerable species variation.
- Some have CNS excitation
- Other species (man) exhibit more depression, disorientation, coma and death (Flu-like symptoms are reported in humans)
- muscle weakness
- elevated heart rate, respiration
- dyspnea
- bright red blood and mucous membranes
- coma and death
30
CO: Treatment
- Place animal on high levels of oxygen to displace carbon monoxide from the hemoglobin
- Respiratory stimulants increase oxygen demand and should be AVOIDED
31
CO and methane are often released from underground sources. What happens if these gases are present at high levels?
- SUFFOCIATION, but have NO biochemical mechanisms that alter Hg or cellular respiration
