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Veterinary Toxicology > Respiratory Toxicology > Flashcards

Respiratory Toxicology Flashcards

1
Q

What are the main causes of toxic exposure in the respiratory system? What 3 characteristics make is more susceptible?

A

inhalation and/or pulmonary circulation

  1. total cardiac output passes through the lungs
  2. thin diffusion barriers that facilitate gas exchange, also facilitate toxicant uptake
  3. large surface area for gas exchange = large surface area for toxicant uptake
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2
Q

What are some pulmonary defenses against toxicants?

A
  • mucus barrier
  • mucociliary escalator system
  • active immune system (BALT)
  • toxicant metabolism
  • high repair capacity
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3
Q

What are the acute and chronic toxic responses of the respiratory system?

A

ACUTE: airway reactivity, edema

CHRONIC: emphysema, fibrosis, asthma, neoplasia

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4
Q

What are the most common signs of respiratory toxicosis?

A
  • coughing
  • nasal discharge
  • epistaxis
  • dyspnea, apnea, hypopnea, hyperpnea
  • increased heart rate
  • grunting
  • weakness, confusion, fatigue, coma, death
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5
Q

What are the 2 most common sources of ammonia (NH3)? What species are especially susceptible?

A
  1. toxic air pollutants in high concentration most common in animal facilities
  2. where feces and other wastes are allowed to accumulate and decompose (poor hygiene)

poultry and pigs

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6
Q

What is the mechanism of toxicity of ammonia? What happens at the high concentrations in animal facilities?

A

NH3 dissolves in aqueous layer in the eye and upper respiratory tract to form NH4OH, which is caustic and causes irritation of the epithelium and necrosis of cells by disrupting cell membrane lipids

chronic stress to the respiratory tract —> secondary bacterial infections and reduced growth

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7
Q

What are the most common clinical signs of ammonia toxicity? What also happens in chicken?

A
  • excessive tearing
  • shallow breathing
  • clear or purulent nasal discharge
  • increased secondary infection, especially Bordetella rhinitis in pigs*
  • reduced production

keratoconjunctivitis, corneal opacity, tracheitis

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8
Q

How can ammonia toxicity be prevented?

A
  • adequate ventilation
  • sanitation
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9
Q

What is carbon monoxide? What are 3 common sources?

A

odorless and colorless gas that is the most common cause of human poisoning in the US

  1. byproduct of incomplete combustion of hydrocarbon fuels, especially in the internal combustion engine
  2. gas water heaters, space heaters, or furnaces in poorly ventilated spaces, like farrowing houses and lambing sheds
  3. fires
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10
Q

What are the 2 mechanisms of toxicity of carbon monoxide? What is the net effect?

A
  1. competes with oxygen for binding sites on hemoglobin (CO = 250x O2), which reduces the carrying capacity of Hb and capacity to give off CO2 in the lungs
  2. increases affinity of O2 for Hb and the stability of O2-Hb bond, which causes the O2 dissociation curve to shit to the left and the release of O2 from Hb is impaired
    - (also affects myoglobin in the same way)

reduced availability of O2 to cells

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11
Q

When will the affinity for oxygen for hemoglobin be high? Decreased? What effect described this?

A

HIGH = decreased temp, decreased pCO2, increased pH, CO, MetHb

LOW = increased temp, increased pCO2, decreased pH

BOHR EFFECT = hemoglobin’s oxygen binding affinity is inversely related both to acidity and to the concentration of carbon dioxide

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12
Q

How does carbon monoxide affect the mitochondria? What does this result in?

A

binds to cytochrome C oxidase in the ETC, which interferes with cellular respiration and causes generation of reactive oxygen species —> oxidative stress

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13
Q

When do clinical signs of carbon monoxide toxicity appear? Death? What do clinical signs reflect?

A

> 25%; > 60%

hypoxia of the tissues - tissues with high oxygen demand (brain, heart, skeletal muscle) are most impacted

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14
Q

What are the initial clinical signs of carbon monoxide poisoning? What is characteristic?

A
  • drowsiness
  • nausea, vomiting
  • lethargy, weakness
  • deafness
  • arrhythmias

cherry-red color to blood, skin, and mucous membranes due to high [COHb]

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15
Q

What is characteristic of severely affected animals undergoing carbon monoxide poisoning? What does chronic low-level exposure lead to?

A
  • dyspnea*
  • terminal clonic spasms
  • coma
  • abortion: CO crosses placental barrier causing fetal hypoxia
  • acute death

exercise intolerance and disturbances in postural and position reflexes

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16
Q

What is the main goal to carbon monoxide poisoning treatment? How is this done?

A

restore adequate oxygen supply particularly to the brain and heart

  • decontaminate with fresh air
  • establish and maintain patent airway with artificial respiration if necessary
  • hyperbaric oxygen
  • blood transfusion of r functional Hb
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17
Q

What is smoke? What materials make the worst smoke?

A

complex mixture of vapors, gases, fumes, heated air, particulates, and liquid aerosols (composition is highly variable)

synthetic materials —> high fume intensity and composition

(inhalation = leading cause of death from fires - carbon monoxide)

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18
Q

What are some adverse effects associated with smoke inhalation?

A
  • thermal injury
  • cyanide exposure
  • inhalation of other noxious gases, aerosols, and particulates
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19
Q

What are the 2 mechanisms of toxicity of smoke inhalation? What clinical signs appear?

A
  1. asphyxiation due to decreased supply and impaired transport of oxygen, occlusion of airway, and central respiratory center depression
  2. irritation of mucous membranes

respiratory compromise and/or systemic toxicity - coughing, dyspnea, tachypnea, tachycardia, dizziness, unconciousness, CNS signs, death

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20
Q

How can radiography be used to diagnose smoke inhalation? What is key to therapy? Why must this be done early?

A

assesses atelectasis, edema, hemorrhage, or infection

maintenance of airway patency —> ET tube intubation or tracheostomy for animals with signs of upper airway injury, obstruction, coma, or burns

developing airway edema can make intubation difficult

21
Q

What drugs are used to treat bronchospasm and bronchoconstriction resulting from smoke inhalation? Cyanide poisoning?

A

β2-adrenergic agonists: Albuterol, Terbutaline, Epinephrine

Hydroxocobalamin

22
Q

What is hydrogen sulfide? What is the most common sources? Where does it tend to accumulte? What species are susceptible?

A

colorless gas with a distinct rotten-egg smell and heavier than air

anaerobic bacterial decomposition of protein and other sulfur-containing organic matter —> manure pits, holding tanks, low areas in animal facilities

swine, cattle, poultry

23
Q

What is the main mechanism of toxicity of hydorgen sulfide? What happens at higher levels?

A

irritation causing inflammation of mucous membranes of the eye and respiratory tract

systemic toxicity (CNS, heart, skeletal muscle) —> stimulates chemoreceptors in the carotid body that maintain arterial pO2, pCO2, and pH, leading to hypernea, acapnia, and apnea; paralyzing effect on respiratory and olfactory centers

24
Q

What clinical signs are associated with hydrogen sulfide toxicity?

A
  • increased secretions in the eye and respiratory tract from irritation
  • pulmonary edema
  • respiratory and olfactory paralysis
  • nervous stimulation (spasms, convulsions)
  • collapse
  • semicomatose state
25
Q

How do humans detect hydrogen sulfide smell?

A

LOW CONCENTRATION = rotten egg

HIGH CONCENTRATION = depressed olfactory sensory apparatus blocks odor detection

26
Q

Why is cardiorespiratory support especially important in hydrogen sulfide toxicity?

A

breathing never re-establishes spontaneously after hydrogen sulfide-induced respiratory paralysis

27
Q

What is paraquat? What are some common sources? What species are most affected?

A

contact herbicide now restricted in the US (used in Canada)

  • contaminated vegetation
  • improperly stored or disposed herbicides
  • access to spills

dogs and cattle

28
Q

Where does paraquat preferentially concentrate? How? How is it excreted?

A

type I and II alveolar cells by diamine-polyamine transport system

largely unchanged in the urine at a speed higher than GFR, meaning it is actively transported

29
Q

What reduces the bioavailability of paraquat? What does this cause?

A

binds tightly to soil —> environmental persistence

30
Q

What are the 2 mechanisms of toxicity of paraquat?

A
  1. irritant and vesicant
  2. redox cycling causes the production of ROS, leading to the oxidation of NADPH and other reductants causing oxidative stress and cell death
31
Q

What are clinical signs of local toxicity due to paraquat? What are the 3 phases of oral exposure?

A

erythema, ulceration, and blistering

  1. irritant/caustic action causes GIT pain, anorexia, vomiting, and diarrhea
  2. renal failure and centrilobular hepatocellular necrosis
  3. pulmonary edema with dyspnea and tachypnea leading to extensive pulmonary fibrosis (poor prognosis)
32
Q

What causes subacute/chronic paraquat toxicosis? How does it manifest? What happens when the animals are exercised?

A

low dose exposure

hyperplasia of type II alveolar epithelial cells with healing by fibrosis

cyanosis due to mismatch between ventilation and perfusion, increased arterial oxygen gradient, and desaturation of Hb with oxygen

33
Q

Where is the highest concentration of paraquat found for diangosis?

A

lung

  • also found in urine and plasma
34
Q

What adsorbent is preferred for paraquat toxicity? Why?

A

activated charcoal > kaolin, clay, bentonite

more effective in reducing the severity and fatality of the toxicosis

35
Q

When can a cathartic be administered following paraquat toxicosis? What additional treatment must be used carefully

A

within 12 hours of exposure —> IV isotonic fluids and diuretics

forced diuresis and charcoal hemoperfusion with Hemocol cartridge - forced diuresis may aggravate pulmonary edema

36
Q

What is contraindicated for treating paraquat toxicosis?

A

supplemental oxygen - aggravates pulmonary damage

37
Q

What does L-tryptophan cause? When does exposure occur?

A
  • acute bovine pulmonary edema and emphysema (ABPE)
  • acute respiratory distress syndrome (ARDS)
  • Fog fever

hungry adult (beef) cattle are moves from dry pastures to rapidly growing, lush, green forage (foggage) high in L-tryptophan

38
Q

What is the pathophysiology of L-tryptophan?

A
  • L-tryptophan is metabolized by ruminal microbes to 3-methylindole, which is absorbed (duodenum) and concentrated in the lungs
  • 3-MI is metabolized by CYP450 or prostaglandin H synthetase in club cells (non-ciliated bronchiolar epithelial cells), macrophages, and type II pneumocytes to the toxic metabolite, 3-methyleneiindolenine
39
Q

How does the toxic principle of L-tryptophan cause toxicity? What are the main 2 results?

A

3-methyleneindolenine preferentially destroys club cells and type I pneumocytes, causing the proliferation of type II pneumocytes that will have a decreased ability to synthesize and secrete surfactant (increased surface tension)

  1. increased alveolar permeability = edema
  2. fibrosis resulting in atypical interstitial pneumonia that does not respond to conventional therapy
40
Q

L-tryptophan pathophysiology:

A
41
Q

When is fog fever most common? What are common clinical signs?

A

late summer, early fall

  • severe dyspnea with open-mouth breathing and reluctance to move
  • standing with feet wide apart, head and neck extended and lowered, and flared nostrils
  • recumbency and death
42
Q

What clinical sign is especially common in less severely affected animals with fog fever? What is not seen?

A

loud expiratory grunting, wheezing, and frothy salivation —> “panters”, “lungers”

coughing and fever

43
Q

What are the 5 most common pathologies associated with L-tryptophan toxicity? What is seen microscopically?

A
  1. heavy, deep purple, glistening cranial lung lobes that do not collapse
  2. firm, rubbery, and distended lungs
  3. air bubbles/gas bullae throughout
  4. pulmonary edema, particularly ventrally
  5. gelatinous yellow fluid oozes from cut surfaces with airways filled

alveolar epithelial proliferation = glandular appearance

44
Q

What are 2 ways that L-tryptophan toxicity can be prevented/controlled?

A
  1. avoid sudden introduction of lush pasture to cattle diet
  2. ionophores may inhibit growth of bacterial tha convert it into 3-MI
45
Q

What are 3 common sources of furans? What species are most affected?

A
  1. perilla ketone from the mint plant, Perilla frutescens
  2. 4-ipomeanol in moldy sweet potatoes infested with Fusarium spp.
  3. peanut vine hay and green beans infested with Fusarium

cattle

46
Q

How is 4-ipomeanol produced in moldy sweet potatoes?

A

Fusarium spp. converts 4-hydroxymyoporone into it under stress

47
Q

Where does the mint plant (Perilla frutescens) commonly grow? When is toxicity risk greatest?

A

around hog pens and in shaded areas along rivers/creeks

late summer, when the flower and seed stage is commonly growing

48
Q

What are the 2 mechanism of toxicity of the mint plant (Perilla frutescens)? What is the most common clinical sign?

A
  1. perilla ketone and 4-ipomeanol damage endothelial cells, which increases permeability and causes edema
  2. destroys type I pneumocytes, causing the formation and proliferation of type II pneumocytes

atypical interstitial pneumonia - acute onset dyspnea with open-mouth breathing, extension of head and neck, loud expiratory grunts, and subcutaneous emphysema along the neck and back with minimal coughing

Veterinary Toxicology (29 decks)

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