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CRH II > RBC Oxidants > Flashcards

RBC Oxidants Flashcards

1
Q

describe acetaminophen

A
  1. OTC analgesic, antipyretic
    -tylenol, generic
  2. prescription meds: lortab, vicodin
  3. dogs and humans:
    -toxicity: 100-900 mg/kg
  4. cats:
    -lower dose for toxicity!
    -40-60mg/kg (deaths at 10mg/kg reported)
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2
Q

describe toxicokinetics of acetaminophen

A
  1. rapid absorption
  2. biotransformation!
    -phase II conjugation
    -dogs: 50-75% glucuronide
    -cats <3%

-phase I oxidation
-deacetylation

  1. excretion: urine
  2. targets: GOOGLE
    -liver: 1ry target
    -dogs and cats: RBCs
    –dogs lack NAT 1, 2
    –cats: NAT1 slow (low glucoronidate)
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3
Q

describe acetaminophen mechanism

A
  1. redox recycling of PAP oxidized Hb to MetHb
  2. reduced activity of reductase
  3. GSH depletion
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4
Q

describe clinical presentation of acetaminophen toxicity

A
  1. 3-12 hours post exposure
  2. decreased O2 transport and hemolytic anemia:
    -cyanosis or dark MM, dyspnea, tachypnea
    -hypothermia, tachycardia
    -hematuria, hemoglobinuria
    -edema and swelling of face and front paws (cats)
    -death
  3. labs:
    -chocolate brown blood
    -methemoglobinemia, heinz bodies
    -elevated liver enzymes
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5
Q

describe treatment of acetaminophen toxicity

A
  1. transfusion, O2 therapy
  2. emesis, activate charcoal with sorbitol
  3. antidote:
    -N-acetylcytseine (glutathione precursor)
    -8 hours post ingestion
  4. others: antidotes with some success
    -sodium sulfate
    -ascorbic acid
    -cimetidine (cytP450 inhibtor)
    -SAMe
    -silymarin
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6
Q

describe nitrate/nitrites

A
  1. nitrate (NO3-); nitrite (NO2-)
  2. found in soil, plants, water: stems and stalks
  3. hay and forage:
    -alfalfa, fescue, sorghum, sudan grass
    -corn, soybean
  4. many poisonous plants
  5. FERTILIZERS:
    -nitrate-based
    -phenoxy herbicides: 2,4 D (dichlorophenoxy acetic acid)
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7
Q

describe target site, species, toxicity, and MOA of nitrate/nitrite

A
  1. target site: hemoglobin
  2. species:
    -nitrate: CATTLE, horses
    -rumen microflora can convert nitrate to nitrite, which then forms MetHb and interferes with O2-carrying capacity of blood
  3. toxicity:
    >10,000 ppm dry weight
    <5000 ppm safe
    5000-10,000: not safe for pregnant cows
    <1,000 ppm in wtaer toxic
  4. MOA:
    -rumen microflora convert, see above
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8
Q

describe clinical presentation of nitrite tox

A
  1. acute: 1-4 hr following rapid ingestion of material high in nitrate
  2. respiratory distress: exercise intolerance, cyanosis, tachypnea, gasping
    -ataxia, tachycardia, seizures, death (6-24hr)
  3. GI distress: salivation, diarrhea
  4. abortion: 3-7 days after sublethal ingestion
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9
Q

describe diagnostics for nitrite tox

A
  1. discolored blood, tissues
  2. Methemoglobinemia
    -may not be evident in animals dead more than a few hours
  3. nitrate/nitrite:
    -blood, urine, ocular fluid
    -hay, water
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10
Q

describe treatment and prevention of nitrite tox

A
  1. reduce MetHgb!!
    -antidote: methylene blue
    -not currently allowed in livestock
  2. reduce ruminal nitrite:
    -cold water lavage
    -ruminal antibiotics: penicillin
    -proprionic bacteria
  3. prevention
    -testing
    -adaptation
    -dilution
    -ensiling
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11
Q

describe onions (and friends)

A
  1. family amaryllidaceae
    -genus allium
    -onions, garlic, shallots, leeks
    -more than 400 species
  2. toxicity:
    -N-propyl disulfides: potent odor
    -varies with plant type, growing conditions, processing, species
    -greater in areas with higher soil SULFUR content: LA, TX, CO, NV, WY, CA
  3. reported poisonings:
    -wild or cultivated
    -raw: fresh or culled
    -dried or dehydrated: minced, flakes
    -cooked: onion souffle, meatloaf
    -powders: baby foods
  4. species:
    -dogs, cats, cattle, horse
    -small ruminants are more resistant
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12
Q

describe onion toxicity MOA

A
  1. plants high in sulfur, when chewed release thiosulfinates
  2. thiosulfinates are converted to disulfides and back and forth
  3. n-propyl disulfides: greatest toxicity
  4. redox recycling of disulfides releases free radicals
    -n-propyl disulfides are oxidants
    -decrease NADPH and GSH
    -RBCs are most sensitive; oxidation of hemoglobin!
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13
Q

describe clinical presentation of onion toxicosis

A
  1. hemolytic anemia
    -acute to delayed onset
    -pale MM, tachypnea, tachycardia, weakness, icterus, hematuria
    -possible vomiting, diarrhea, anorexia
  2. labs: anemia, hemoglobinemia, HEINZ BODIES
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14
Q

describe treatment of onion toxicosis

A
  1. blood transfusion
  2. fluids
  3. GI decontamination
    -emesis: if NOT vomiting
    -activated charcoal
  4. monitor hematocrit for several days!
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15
Q

describe zine

A
  1. an essential nutrient
  2. sources:
    -pennies before 1982
    -skin ointments
    -galvanized metals: bolts, nails
    -paints (55%)
    -dietary excess
  3. monogastrics: dogs and pigs
  4. birds
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16
Q

describe toxicokinetics of zinc

A
  1. absorption:
    -upper small intestine: Zn2+
    -increased by dietary Zn deficiency
    -acidic pH
  2. distribution:
    -transport proteins
    -liver: release back to circulation
    -accumulation: liver, pancreas, muscle, bone
  3. excretion:
    -feces: bile, pancreatic fluids, GI mucosa
17
Q

describe zinc MOA and toxicosis

A

MOA:
-oxidative damage
-Heinz bodies
-RBC hemolysis

toxicosis:
-initial: gastroenteritis
-hemolytic anemia: icterus, tachycardia, hemoglobinuria, renal failure

18
Q

describe treatment of zinc toxicosis

A
  1. fluids, transfusions
  2. remove source
  3. antacids: metallic Zn
  4. H2 antagonists: increase pH, decrease absorption

5, chelation!
-Ca2+ disodium EDTA

19
Q

describe methylxanthines

A
  1. origin:
    -plant alkaloids found in chocolate, coffee, tea, cola
    -3 alkaloids: theobromine, caffeine, theophylline
  2. other sources:
    -cocoa bean shell mulch
    -OTC meds/stimulants, herbal
    -human and veterinary medications!
20
Q

describe chocolate

A

80% theobromine, 20% caffeine

-baking chocolate has highest levels of theobromine!! followed by dark chocolate, then milk chocolate

21
Q

describe methylxanthine toxicosis in dogs and cats

A
  1. LD50: 80-200mg/kg
    -mild signs: 20 mg/kg
    -severe signs: 40-50 mg/kg
    -seizures: 60 mg/kg

AKA toxicity with
1 ounce milk chocolate per pound BW or
0.1oz backers chocolate per pound body weight

longer half life in dogs = bigger window of opportunity

22
Q

describe toxicokinetics of methylxanthines

A
  1. absorption/distribution:
    -readily absorbed
    -widely distributed
    -crosses placenta
  2. elimination:
    -biotransformation: phase I and II to inactive metabolites
  3. excretion:
    -bile; reabsorption
    -urine: reabsorption from bladder
    -milk
23
Q

describe methylxanthine MOA

A
  1. complete antagonists of adenosine receptors

adenosine: nucleoside,
-in ATP for energy transfer

-in cAMP for signal transduction as phosphodiesterae inhibitors (non-competitive, regulate cAMP level)

-inhibitory neurotransmitter to allow sleep

  1. adenosine binds to
    A1 receptors: decrease HR, decrease force of atrial contraction, and respond to epinephrine
    -decrease CNS excitability, inhibit EAA release
    -anti-diuretic

A2 receptors: regulate vascular tone, dilate coronary arteries

24
Q

describe clinical presentaion of methylxanthine toxicosis

A

depends on what ingested and how much!!

dogs and cats:
-1-12 hours post ingestion

-polydipsia, vomiting, bloating, diarrhea

-hyperactivity, polyuria, tremors, seizures

-tachycardia, arrhythmias, tachypnea, cyanosis, hypertension

-hyperthermia, coma

-death (cardiac failure) is rare

25
Q

describe treatment of methylxanthine toxicosis

A
  1. stabilize:
    -tremors and seizures: methocarbamol, diazepam

-antiarrhythmia drusg!!

  1. GI decontamination:
    -emetics or gastric lavage
    -activate charcoal, repeated
    -1x cathartic
  2. fluid therapy
  3. urinary catheter to prevent reabsorption from bladder
  4. severe cases:
    -72 hours to resolve
    -24-72 hours: pancreatitis could follow due to increased fat consumption from original ingestion (choccy)
26
Q

describe TCAs

A
  1. antidepressants used for chronic pain
    -amitryptiline, nortriptyline, imipramine
    -min LD <15 mg/kg
  2. toxicokinetics:
    -lipophilic: rapidly absorbed and widely distributed
    -peak plasma levels within 2 hours
    -liver biotransformation, urinary excretion: some active metabolites, some enterohepatic circulation
27
Q

describe TCA MOA

A

multiple!

  1. block reuptake of dopamine, NE, 5-HT
  2. anticholinergic activity
  3. antihistaminergic activity
  4. anti alpha-adrenergic activity
28
Q

describe clinical presentation and treatment of TCA toxicosis

A

clinical presentation:
1. rapid onset: 30 min (bc lipophilic)

  1. lethargy, ataxia
  2. progress to tachycardia, mydriasis, vomiting, hypotension, cardiac arrhythmias, dyspnea, pulmonary edema, seizures, hyperthermia, coma, death
  3. death within 1-2 hours

treatment:
1. no antidotes!

  1. CV: fluid therapy for hypotension, hyperthermia
    -arrhythmias will resolve in most cases
  2. CNS: diazepam
  3. GI decontamination:
    -skip emesis, go to gastric lavage
    -activated charcoal with sorbitol, repeat AC only
29
Q

describe amphetamines

A

sources:
-prescription: CNS stimulant, appetite suppressants, mood enhancers
-illegal drug use

formulation:
-tablets
-alkaline
-derivatives: methamphetamine; ecstasy (MDMA)

toxicity:
-approximate oral LD50: 10-30 mg/kg

30
Q

describe amphetamines toxicokinetics

A
  1. absorption:
    -alkaline drugs
    -rapid intestinal absorption
    -peak levels reached within 2-3 hours
  2. distribution: rapid and wide
  3. elimination:
    -biotransformation: liver
    -excretion: urine
31
Q

describe amphetamines MOA

A
  1. potentiates catecholamine release
    -CNS: adrenal gland
    -NE: dopamine
  2. inhibit monoamine oxidase
  3. block NE-DA re-uptake
32
Q

describe amphetamine tox clinical presentation

A
  1. rapid onset: 1-2 hr
  2. hyperexcitability, agitation, mydriasis, tremors, hyperreflexia, rapid breathing
  3. tachycardia, hypertension, cardiac arryhthmias
  4. infrequent seizures
33
Q

describe amphetamine tox treatment

A
  1. stabilize:
    -control hyperactivity: diazepam, barbiturates

-control cardiac arrhythmias

  1. decontamination:
    -emetics, lavage, activated charcoal, cathartic

CRH II (53 decks)

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