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Toxicology > Toxic gases > Flashcards

Toxic gases Flashcards

1
Q

what happens when ammonia comes in contact with MM?

A
  • forms ammonium hydroxide which is irritating and caustic
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2
Q

how does an animal become exposed to ammonia?

A
  • inhalation***
  • environmental conditions
  • decomposing manure in confined animal houses
  • burning plastics
  • used in agricultural fertilizer
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3
Q

at what level of NH3 will eyes burn?

A

25-35ppm

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4
Q

what exposure of NH3 can cause acute death?

A

5000ppm

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5
Q

what are the toxicokinetics of NH3?

A
  • converted to a strong base irritant (ammonium hydroxide) on MM
  • primarily absorbed by inhalation and is distributed to tissue cells
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6
Q

what is the MOA of NH3?

A
  1. direct irritation of MM
  2. causes pulmonary edema and lung congestion
    3 alkalosis and compensatory acidosis
  3. inhibit TCA cycle
  4. increased susceptibility can lead to resp infections due to continuous exposure - irritation - inflammation - secondary infections
    - 50-75ppm: decreased ability to clear bacteria from the lungs –> resp dysfunction
  5. decreased growth of young animals
    - 100ppm: decreased growth rate by 32% in swine
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7
Q

what are the CS with acute NH3 toxicity?

A

red MM, lacrimation, coughing, sneezing, nasal discharge, keep eyes shut

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8
Q

what are the CS with chronic NH3 toxicity?

A
  • decreased growth rate and production

- dyspnea - fluid in the lungs caused by pulmonary edema/congestion

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9
Q

what are the CS with terminal NH3 toxicity?

A

CNS stimulation, clonic convulsions, cyanosis

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10
Q

how do we diagnose NH3 toxicity?

A
  • history
  • odor of ammonia
  • CS
  • lesions (blisters on MM)
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11
Q

how do we treat NH3 toxicity?

A
  • remove source
  • fresh air
  • soothing ointments for eyes
  • antibiotics may prevent secondary infections
  • diuretics for pulm edema
  • treat any secondary infections
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12
Q

what are the main properties of hydrogen sulfide gas (H2S?)

A
  • colorless
  • odor of rotten eggs
  • heavier than air
  • flammable
  • water soluble
  • irritant because converted to sulfuric acid
  • forms black or dark colored compounds in GIT and tissues
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13
Q

what are the main routes of exposure for H2S?

A
  • INHALATION
  • by product or waste material from industry **
  • may be liberated in coal pits, gas wells, or sulfur springs
  • also associated with natural gas and crude oil production
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14
Q

humans can detect H2S at what level?

A

0.025ppm

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15
Q

at what level does H2S cause eye irritation?

A

20ppm

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16
Q

at what level is H2S possibly fatal?

A

400ppm

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17
Q

what does 1000ppm H2S cause?

A

rapid unconsciousness and death in about 1 hour

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18
Q

> 2000ppm H2S cause what?

A

resp paralysis after 1-2 breaths

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19
Q

what are the toxicokinetics of H2S?

A
  • readily absorbed through the lungs and GIT
  • converted to alkali sulfides in the blood
  • hydrosulfide radical is normally oxidized to sulfate and is excreted in urine
  • some sulfide is excreted in feces
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20
Q

what is the MOA of H2S?

A
  • direct irritation of MM
  • inhibition of cellular respiration
  • decreased cytochrome oxidase
  • stimulation of the chemoreceptorsof the carotid body - depressed resp drive
  • DIE FROM ASPHYXIATION
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21
Q

what are the CS from acute H2S exposure?

A
  • sudden collapse
  • cyanosis
  • dyspnea
  • convulsions
  • rapid death
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22
Q

what are the CS from chronic H2S exposure?

A
  • eye, resp, and lung irritation
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23
Q

what are the CS from chronic H2S exposure?

A
  • eye, resp, and lung irritation
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24
Q

what are the lesions associated with H2S poisoning?

A
  • blood is dark and may not clot
  • tissues may be dark or greenish purple
  • carcass may have sewage odor
  • if ingested, the GI contents may be black or dark gray and smel of sewage
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25
Q

how do we treat H2S toxicity?

A
  • removal of source
  • sodiun nitrite IV may be partly effective by forming methemoglobin - binds sulfide radicals and reactivates cytochrome oxidase
  • oxygen therapy, ventilation
  • educate about prevention (get H2S monitors!)
26
Q

what are the properties of carbon monoxide (CO)?

A

odorless, colorless, not water soluble

27
Q

what are common exposure routes for CO?

A
  • accidental exposure with fires (incomplete combustion of carbon containing products - wood, paper, petroleum products)
  • propane powered equipment, space heaters, portable cookers, de-icers
  • automobile exhaust in confined spaces
28
Q

what is the MOA of CO?

A
  • CO combines with hemoglobin to form carboxyhemoglobin and reduced the level of O2 (hemoglobin has a 240x higher affinity for CO)
  • carboxyhemoglobin interferes with release and availability of O2 carried by hemoglobin
  • some intereference with cellular resp
  • also competes with O2 for binding sites on myoglobin
29
Q

what is death due to from CO poisoning?

A

hypoxia

30
Q

what are the main CS with CO poisoning?

A
  • sudden death at 60-70% COHb

- in low exposure (30-60% COHb) signs = hypoxia, drowsiness, incoordination, dyspnea, lethargy, coma

31
Q

what are the lesions associated with CO toxicity?

A
  • blood is bright red and the MM are pink
  • no significant lesions in acute cases
  • in chronic cases there may be brain edema, hemorrhage, and necrosis which may cause deafness in dogs/cats
32
Q

what lab diagnostics can we run to confirm CO toxicity?

A
  • measuring CO in air

- percentage of COHb in the blood (correlation to CS is poor)

33
Q

how do we treat CO toxicity?

A
  • oxygen or 5% CO2 in oxygen administered with positive pressure
  • blood transfusion
  • fluid for acidosis but bicarb use is controversial
34
Q

what are the common sources of Nitrogen Oxide gases?

A
  1. farm
    - NO2 and N2O4 gases are produced by incomplete reduction of nitrates during fermentation process in silo’s
    - nitrogen oxide poisoning = Silo filler’s disease
  2. industry
    - NO2 is a major pollutant (burning of fossil fuels)
35
Q

what are the major properties of Nitrogen Oxide gases?

A
  • NO2 gas is reddish brown
  • N2O4 is colorless
  • NO2 is heavier than air but the gases are about as dense as air - forms layers on top of silage and settles down on the chute
  • gas mixture has an irritating chlorine-like odor
  • low solubility in water
36
Q

which nitrogen oxide gas exposure is more toxic - acute or chronic?

A

acute

37
Q

what are the toxicokinetics of nitrogen oxide gases?

A
  • animal quarters that develop the irritant odor or yellow haze in the air must not be entered
  • nitrogen dioxide and tetraoxide gases form nitric acid upon contact with mucus membranes
  • cross resp mucosa and cause cellular damage in the lungs - pulmonary edema
38
Q

what is the MOA of nitrogen oxide gases?

A
  • direct irritation of the MM by nitric acid
  • low water solubility - passes from upper to lower resp tract and causes damage in the lungs
  • lung damage - due to caustic reaction with the PFAs at cellular membrane - pulmonary edema, hemorrhage
  • death is from hypoxia -resp failure
39
Q

what are the CS associated with nitrogen oxide gas toxicity?

A
  • resp signs - generally similar to ammonia poisoning (irritation of MM, effects on respiration)
40
Q

what lesions are associated with nitrogen gas toxicity?

A
  • pulmonary edema
  • hemorrhage
  • emphysema
  • cyanosis
  • methemoglobinemia
  • necrosis of skeletal muscle
41
Q

how do we treat nitrogen oxide gas toxicity?

A
  • supportive treatment
  • diuretics if pulmonary edema
  • methylene blue IV for methemoglobinemia
  • antibiotic ointment for MM
42
Q

at what percentage of methemoglobinemia do we normally start seeing toxic signs?

A

15% (normal is 1%)

43
Q

what are the common sources of exposure with sulfure oxide gases?

A
  • sulfur dioxide SO2 and sulfur trroxide (SO3) are industrial pollutants
  • fossil fuel combustion at power plants
44
Q

what are the main properties of sulfur oxide gases?

A
  • highly soluble in water
  • sharply irritant to MM because the form sulfurous and sulfuric acids on contact with water
  • odor causes coughing, choking, and suffocation
45
Q

SO2 at ___ppm is fatal to cats within 30-60mins

A

500

46
Q

SO2 at 500ppm for __ hour(s) is dangerous to grazing animals

A

1

47
Q

SO2 at ___ppm for 8 days causes poisoning in pigs

A

5-40

48
Q

what is the MOA of sulfur oxide gases?

A
  • direct irritation of the MM - primarily upper resp tract
  • reflex bronchoconstriction - lung damage
  • death due to hypoxia
49
Q

what are the CS and lesions associated with sulfur oxide gas toxicity?

A
  • similar to other toxic gases (irritation to MM, effects on respiration)
50
Q

what all does “smoke” include?

A

vapors, gases, fumes, heated air and particulate matter, liquid and solid aerosols

51
Q

why is there no LD50 for smoke?

A

it is a heterogenous mixture of gases - too many variable

52
Q

inhalation of super-heated air and steam can cause?

A

thermal burns to resp tract and enhance absorption of gases

burns in the resp tract enhances toxicity

53
Q

what are the MOAs of smoke inhalation?

A
  1. simple asphyxiants - inert (CO2) gases or vapors displace O2
    - low concentration, generally have little if any physiological effect
  2. chemical asphyxiant - prevent uptake of O2
    - produce toxic local (lungs) and systemic effects
    - carbon monoxide –> COHb
  3. irritants
    - chemically reactive on contact with MM to cause local effects
    - sulfur dioxide –> sulfuric acid
    - particle - ash and soot
54
Q

what are the CS associated with chemical asphyxiants?

A
  1. resp
    - cough, dyspnea, tachypnea
    - wheezing, decreased breath sounds, crackles
  2. CV
    - tachycardia, hypoxemia
    - hypotension, dysrhythmias
  3. signs of irritation
    - conjunctivitis, pharyngitis, rhinitis, drooling, hoarseness
    - edema, mucosal ulcerations
    - corneal abrasions common from ash/soot
  4. CNS
    - agitation, confusion, ataxia, abnormal posture, seizure
  5. surface burns
55
Q

what kind of lesions might we see with smoke inhalation (chemical asphyxiants?)

A
  • burns
  • pulmonary changes
  • cerebral edema
56
Q

how do we treat smoke inhalation (chem asphyxiants)?

A
  • prompt removal from the smoke environment + O2 support
  • B2 adrenergic agonists may benefit for bronchoconstriction
  • NO STEROIDS
  • remove soot from skin
  • avoid cough suppressants and opioids
  • maintain airway patency, ventilation, etc
57
Q

____ of the toxin (gas, chemical) is the most importany determinant of resp injury

A

solubility

58
Q

highly soluble particles (smoke inhalation) end up where in the resp tract?

A

upper airway

- injury to the mucosa, inflammatory mediators, free radicals –> increased permeability –> edema

59
Q

low water soluble particles (smoke inhalation) end up where in the resp tract?

A
  • lung, bronchiole, alveoli

- slower reaction, delayed effect

60
Q

ammonia and sulfur dioxide have high or low water solubility?

A

high - end up in upper airway

- chemically reactive on contact with mucus

61
Q

nitrogen oxides have high or low water solubility?

A
  • low - end up in pulmonary parenchymal injury in the alveoli, alveolar ducts

Toxicology (12 decks)

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