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Toxicology > Heavy metals (Bergfelt)--toxic gases > Flashcards

Heavy metals (Bergfelt)--toxic gases Flashcards

1
Q

What are possible sources of ammonia toxicity?

A
  • Decomposing manure in confined animal houses
  • Burning nylon/plastics
  • Anhydrous ammonia used in agricultural fertilizer
    • Transported, applied under high pressure
    • Broken hoses/valves
    • Formation of a vapor cloud
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2
Q

T/F: Ammonia has a characteristic sharp odor and is heavier than air

A

TRUE

Anhydrous gas is lighter than air but in the presence of moisture forms vapors that are heavier

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3
Q

Is ammonia soluble in water?

A

Yes

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4
Q

What does ammonia react with in mucous membranes?

A

Readily reacts with hydroxyl ions in moist mm to form ammonium hydroxide, which is irritant and caustic

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5
Q

Where are high concentrations of ammonia most frequently found?

A

Animal houses–may reach 50ppm during normal operations

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6
Q

Which animals are more susceptible to ammonia toxicity?

A

Livestock (swine, poultry)

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7
Q

What level of ammonia can cause acute death?

A

Exposure to 5000ppm

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8
Q

What is ammonia converted to on mucous membranes?

A

A strong irritant (ammonium hydroxide)

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9
Q

How is ammonia absorbed/distributed?

A

By inhalation and is distributed to tissue cells

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10
Q

Ammonia toxicity increases susceptibility to what?

A

Respiratory infections due to continuous irritation

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11
Q

At what level will ammonia decrease an animal’s ability to clear bacteria from the lungs?

A

50-75ppm

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12
Q

At what level will ammonia decrease growth in young animals?

A

100ppm: decreased growth rate by 32% in swine and additive w/ other causes (ascarid infection)

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13
Q

What does inhalation of large ammonia concentrations cause?

A

Pulmonary edema and lung congestion due to increased permeability of lung capillaries

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14
Q

T/F: Ammonia toxicosis causes acidosis and compensatory alkalosis

A

FALSE–it causes alkalosis and compensatory acidosis

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15
Q

T/F: Ammonia toxicosis may inhibit the TCA cycle

A

TRUE

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16
Q

What might death of ammonia toxicosis be due to?

A

May be partly due to asphyxia and partly due to electrolyte and cellular metabolic effects

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17
Q

What are the clinical signs associated w/ ammonia toxicosis?

A
  • Red mucous membranes, lacrimation, coughing, sneezing, nasal discharge (serous and mucous), keeping eyes shut
  • Decreased growth rate and dec. egg production in birds
  • Dyspnea, poss. fluid in lungs due to pulmonary edema
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18
Q

What terminal signs are assoc. w/ ammonia toxicosis?

A

Cyanosis, CNS stimulation, and clonic convulsions

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19
Q

T/F: Chemical analyses are not routinely made with toxic gases

A

TRUE

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20
Q

DDx for ammonia toxicosis?

A
  • Diseases that cause respiratory insufficiency
    • Inhaled irritants (hydrogen sulfide, nitrogen oxides, sulfur oxides, fumes, dusts, vapors)
    • Organophosphates
    • Polychlorinated biphenyls
    • Cardiac glycosides
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21
Q

Treatment for ammonia toxicosis?

A
  • Removal of the source and animal
    • Premises must be kept clean and well-ventilated
  • Fresh air is a good treatment for dyspnea
  • Soothing ointments applied to the eyes
  • Antibiotics may prevent secondary infections
  • Diuretics for pulmonary edema
  • Treat any secondary infections (pneumonia)
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22
Q

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

A
  • H2S, NH3, CO2, and methane are liberated from decomposition of urine and feces in underfloor waste pits, deep litter, manure packs, sewage, and other organic matter containing sulfur
  • By-product or waste from industrial industry
  • May be liberated in coal pits, gas wells, or sulfur springs
  • Liquid manure holding pits (swine)
  • Also assoc. w/ natural gas and crude oil production, some coal-deposits, by-product of some industrial applications, and burning rubber
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23
Q

Why are liquid manure holding pits (swine) dangerous?

A
  • H2S is retained in the liquid within the pit
  • Released when liquid is agitated (to pump)
  • Normal H2S levels ~10ppm
    • When slurry is agitated may reach 1000ppm
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24
Q

T/F: H2S is the most dangerous sewage gas

A

TRUE

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25
Q

What are the various levels of H2S that cause problems?

A
  • 0.025ppm = human detection in air
  • 20ppm = ocular irritation
  • 50ppm = severe symptoms
  • 200ppm = olfactory accommodation (danger)
  • Sudden exposure to 400ppm may be quickly fatal
  • 1000ppm = rapid unconsciousness and death in about 1hr
26
Q

T/F: Acute H2S poisoning is directly responsible for more deaths in closed animal facilities than any other gas

A

TRUE

27
Q

T/F: Most mammal’s susceptibility to H2S is similar

A

TRUE: acute toxic levels ~500-800ppm

Poultry 4000ppm did not result in immediate death

28
Q

Where is H2S readiy absorbed through?

A

Lungs and GIT

29
Q

What is H2S converted to in the blood?

A

Alkali sulfides

30
Q

What happens to the hydrosulfide radical?

A

It is normally oxidized to sulfate and excreted in urine

31
Q

T/F: Some sulfides may be trapped by natural disulfides (i.e. glutathione) in the blood while some sulfide is excreted in feces as iron sulfide

A

TRUE

32
Q

How does H2S inhibit cellular respiration?

A

By inhibiting cytochrome oxidate

(50-100ppm = permanent effects on NS)

33
Q

What does H2S stimulate?

A

Chemoreceptors of the carotid body interfering with the respiratory drive

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

>2000ppm = respiratory paralysis after 1-2 breaths

34
Q

What are the clinical signs associated with H2S toxicosis?

A
  • Large concentrations may cause sudden collapse, cyanosis, dyspnea, anoxic convulsions and rapid death
  • Lower concentrations = signs of irritation to ocular, respiratory mucosa and lungs as in ammonia
35
Q

Lesions associated with H2S toxicosis?

A
  • Dark blood that may not clot
  • Tissues might be dark or greenish purple (reaction w/ iron, etc.)
  • Carcass may have odor of H2S (sewage)
  • If ingested the GI contents may be black or dark grey and have sewage odor
36
Q

What are 3 main properties of H2S?

A
  • Colorless, smells of rotten eggs
  • Heavier than air
  • Flammable
37
Q

What other metals does H2S react with?

A

Reacts with Ag, Fe, Pb, and other metals to form black or dark-colored compounds (in the GIT and maybe in tissues)

38
Q

What are the DDx for H2S toxicosis?

A

Same for ammonia

39
Q

Treatment of H2S toxicosis?

A
  • Removal of source
  • Sodium nitrite IV may be partly effective by forming methemoglobin that binds the hydrated sulfide radical and reactivate cytochrome oxidase
  • The hydrated sulfide anion can interact with disulfides such as oxidized glutathione
  • Oxygen therapy, ventilation, supportive treatment,
40
Q

T/F: If an animal is ventilated until blood H2S levels go down it can recover from H2S toxicosis

A

TRUE

41
Q

Management of H2S toxicosis?

A
  • Monitor animals when agitation of pit started
  • If clinical signs show, shut off pump
  • Do not rescue animals immediately (risk of human exposure)
  • Prevention is most effective treatment
42
Q

T/F: H2S is included in the ‘recipe for flatus’

A

TRUE

43
Q

Sources of CO toxicosis?

A
  • Accidental exposure by CO from fires
    • Incomplete combustion of C-containing products (wood, paper, petroleum products)
  • Propane powered equipment, space heaters, portable cookers, driveway de-icers, etc.
  • Automobile exhaust in confined spaces
    • Modern emissions 0.5%, more in diesel
44
Q

T/F: CO is odorless and colorless

A

TRUE

45
Q

Is CO toxicosis common?

A

No–may be occasional toxicosis in dogs, cats, chickens, or livestock

46
Q

What does the phrase “canary in a coal mine” refer to?

A

Smaller animals have faster breathing rates and smaller Vd–may show toxicity before humans

47
Q

What levels of CO can cause clinical signs and death w/in 1hr of exposure?

A

>1000ppm (0.1%)

48
Q

T/F: The fetus is less sensitive to CO levels

A

FALSE–fetus is more sensitive

49
Q

What does CO combine with in the body?

A

Hemoglobin to form carboxyhemoglobin (COHb) which cannot carry oxygen

(Hemoglobin affinity for CO is 240x greater than for O2)

50
Q

After its formation, what does carboxyhemoglobin interfere with?

A

Interferes with the release of oxygen carried by normal hemoglobin

  • Increases stability of the Hb-O2 bond
  • “Haldane effect” = increased affinity for O2
  • Leftward shift of O2 dissociation curve
51
Q

What causes death following CO toxicosis?

A

Hypoxia

52
Q

T/F: CO also competes with O2 binding sites on myoglobin which is worsened in hypoxia

A

TRUE

53
Q

At what level does CO interfere with cellular respiration?

A

Mitochondrial level

Can lead to free radical formation and attachment to leukocytes

54
Q

What are the clinical signs associated with CO toxicosis?

A
  • Sudden death
  • In low exposure (30-60% COHb) signs are hypoxia, drowsiness, incoordination, dyspnea, lethargy, coma
  • Moderate concentrations (<250ppm) = increased number of stillborn fetuses in swine farrowing houses or lambing barns
55
Q

Death occurs at what % COHb?

A

60-70%

Breathing 13% CO for 1 hour

56
Q

T/F: In low exposure clinical signs can be very nonspecific

A

TRUE

57
Q

What are the lesions in CO toxicosis?

A
  • Bright red blood with healthy pink mm
    • Carboxyhemoglobin is bright red + hyperventilation
    • Don’t always see this
58
Q

What lesions are seen in acute CO toxicity cases? What about chronic cases?

A
  • No significant lesions in acute cases
  • In chronic cases there may be brain edema, hemorrhage, and necrosis which may cause deafness in dogs and cats
59
Q

Laboratory diagnosis for CO toxicity?

A
  • Measure CO in air
  • Percentage of carboxyhemoglobin in the blood
    • Carboxyhemoglobin in whole blood is stable for several days if refrigerated
    • Correlation to clinical signs is poor
    • COHb conc. in fetal thoracic fluid (>2%)
60
Q

What is the treatment for CO toxicosis (if there’s time)?

A
  • O2 or 5% CO2 in O2 administered w/ positive pressure
    • O2 to displace CO
    • O2 by mask/chamber/tube
      • 100% O2 (not for more than 18hrs)
    • Hyperbaric O2?
    • CO2 induced hyperpnea
  • Blood transfusion
  • Fluids for acidosis but bicarbinate use is controversial (may affect O2 dissociation curve)
61
Q

T/F: Recovery may or may not occur even after treatment for CO toxicosis

A

TRUE

Toxicology (22 decks)

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