Heavy metals (Bergfelt)--toxic gases Flashcards Preview

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Flashcards in Heavy metals (Bergfelt)--toxic gases Deck (61)
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1

What are possible sources of ammonia toxicity?

  • 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

2

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

TRUE

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

3

Is ammonia soluble in water?

Yes

4

What does ammonia react with in mucous membranes?

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

5

Where are high concentrations of ammonia most frequently found?

Animal houses--may reach 50ppm during normal operations

6

Which animals are more susceptible to ammonia toxicity?

Livestock (swine, poultry)

7

What level of ammonia can cause acute death?

Exposure to 5000ppm

8

What is ammonia converted to on mucous membranes?

A strong irritant (ammonium hydroxide)

9

How is ammonia absorbed/distributed?

By inhalation and is distributed to tissue cells

10

Ammonia toxicity increases susceptibility to what?

Respiratory infections due to continuous irritation

 

11

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

50-75ppm

12

At what level will ammonia decrease growth in young animals?

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

13

What does inhalation of large ammonia concentrations cause?

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

14

T/F: Ammonia toxicosis causes acidosis and compensatory alkalosis

FALSE--it causes alkalosis and compensatory acidosis

15

T/F: Ammonia toxicosis may inhibit the TCA cycle

TRUE

16

What might death of ammonia toxicosis be due to?

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

17

What are the clinical signs associated w/ ammonia toxicosis?

  • 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

18

What terminal signs are assoc. w/ ammonia toxicosis?

Cyanosis, CNS stimulation, and clonic convulsions

19

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

TRUE

20

DDx for ammonia toxicosis?

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

21

Treatment for ammonia toxicosis?

  • 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)

22

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

  • 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 

23

Why are liquid manure holding pits (swine) dangerous?

  • 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

24

T/F: H2S is the most dangerous sewage gas

TRUE

25

What are the various levels of H2S that cause problems?

  • 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

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

TRUE

27

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

TRUE: acute toxic levels ~500-800ppm

Poultry 4000ppm did not result in immediate death

28

Where is H2S readiy absorbed through?

Lungs and GIT

29

What is H2S converted to in the blood?

Alkali sulfides

30

What happens to the hydrosulfide radical?

It is normally oxidized to sulfate and excreted in urine

31

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

TRUE

32

How does H2S inhibit cellular respiration?

By inhibiting cytochrome oxidate

(50-100ppm = permanent effects on NS)

33

What does H2S stimulate?

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

What are the clinical signs associated with H2S toxicosis?

  • 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

Lesions associated with H2S toxicosis?

  • 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

What are 3 main properties of H2S?

  • Colorless, smells of rotten eggs
  • Heavier than air
  • Flammable

37

What other metals does H2S react with?

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

38

What are the DDx for H2S toxicosis?

Same for ammonia

39

Treatment of H2S toxicosis?

  • 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

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

TRUE

41

Management of H2S toxicosis?

  • 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

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

TRUE

43

Sources of CO toxicosis?

  • 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

T/F: CO is odorless and colorless

TRUE

45

Is CO toxicosis common?

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

46

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

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

47

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

>1000ppm (0.1%)

48

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

FALSE--fetus is more sensitive

49

What does CO combine with in the body?

Hemoglobin to form carboxyhemoglobin (COHb) which cannot carry oxygen

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

50

After its formation, what does carboxyhemoglobin interfere with?

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

What causes death following CO toxicosis?

Hypoxia

52

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

TRUE

53

At what level does CO interfere with cellular respiration?

Mitochondrial level

Can lead to free radical formation and attachment to leukocytes

54

What are the clinical signs associated with CO toxicosis?

  • 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

Death occurs at what % COHb?

60-70%

Breathing 13% CO for 1 hour

56

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

TRUE

57

What are the lesions in CO toxicosis?

  • Bright red blood with healthy pink mm
    • Carboxyhemoglobin is bright red + hyperventilation
    • Don't always see this

58

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

  • 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

Laboratory diagnosis for CO toxicity?

  • 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

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

  • 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

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

TRUE