10: Toxicant Affecting Cardiac/Resp Systems 2

datura stramonium

jimsonweed

atropa belladonna

deadly nightshade

toxic principles of solanceae

hyoscyamine, scopolamine, atropine (d/I-hyoscyamine)

MoA of solanceae

inhibits PNS

Zigadenus spp

death camas

toxic agent of death camas

zigacine

signs of zigacine toxicity

death from severe vasodilation/bradycardia, cardiac necrosis, CNS involvement

Ageratina spp

white snakeroot (formerly Eupatorium)

toxic principle of white snakeroot

tremetone/Tremetol (mixture of ketones)

toxicokinetics of tremetone

must be activated by microsomal enzymes, toxic agents found in milk

signs of tremetone toxicity

weakness, tremors, cardiac/skeletal muscle damage, acetone smell to breath

components of gas exchange between ENVIRONMENT AND AIRWAYS

respiratory muscles, CNS, chemo-mechano receptors

components of gas exchange between AIRWAYS AND BLOOD

airways, alveoli, vasculature, fibrous network

acute airway reactivity

bronchoconstriction (asthmatic)

acute lung injury

pulmonary edema

what can cause fatal pulmonary edema in pigs 1-4 hours after exposure?

fumonisin

toxic gases

chlorine/chloramine, ammonia, CO, methane, hydrogen sulfide

chlorine/chloramine gases

irritate upper airways, 30-90 minutes

how to make choramine

rxn of ammonia with sodium hypochlorite

ammonia about 100 ppm

irritate eyes/respiratory membranes, increases parasitic infection INTENSTIY, reduces growth rate chronically

true or false: CO binds hemoglobin with HIGHER AFFINITY than O2

TRUE

when is methane an asphyxiant?

85%

greatest danger of hydrogen sulfide

paralyzing respiratory tract

characteristics of hydrogen sulfide gas

heavier than air, insoluble in water

what can cause pulmonary edema and hemorrhages in birds?

PTFE-coated cookware, used at temps higher than 536 degrees

conium maculatum

poison hemlock

cicuta douglasii

water hemlock

toxic principle of poison hemlock

N-methyl coniine, coniine

MoA of coniine toxin (poison hemolock)

blocks neuromuscular junctions

signs of coniine toxicity (poison hemlock)

rapid progressive muscle weakness, paralysis, resp failure

toxic principle of water hemlock

cicutoxin

MoA of cicutoxin (water hemlock)

inhibits GABAergic receptors

ABPEE

acute bovine pulmonary emphysema and edema

when does ABPEE occur?

fall, 5-10 days after change to lush pasture

toxicant causing ABPEE

metabolites of AA L-tryptophan (naturally occurring in diet, coverted to toxin in rumen)

perilla frutescnens

perilla mint

toxin of perilla mint

perilla ketone

toxin of moldy sweet potatoes

aflatoxin 4-ipomeanol

MoA of perilla ketone (perilla mint)

damages pulmonary endothelium and type I pneumocytes, proliferating type II pneumocytes

what do type I pneumocytes do?

gas exchange

what do type II pneumocytes do?

produce surfactant, can go back to type I but takes time

clinical sings of perilla mint/moldy sweet potato intoxication

ABPEE and other pneumonia signs

prunus spp and sorghum spp

cytogenic plants

prunus spp usually affects

SA

sorghum spp usually affects

LA

cytogenic fruits

wild/choke cherries, apricot, peach, apple (things with pits)

cytotoxic grasses

johnson, arrow, sudan grasses

most common toxins in cyanogenic plants

amygdalin and prunasin

toxicokinetics of amygalin and prunasin (cyanogenic plant toxins)

converted to HCN in GI tract and absorbed

why are SA uncommonly affected by cyanogenic plant toxicitiy?

have to crush fruit pits in GI tract and most SA this is very hard to do!

if animal has consumed cyogenic plant and is alive, will they be okay?

YES! death occurs by CRUSHING PITS/PLANTS and happens VERY QUICK. if animal is alive/made it to vet, they will be okay

MoA of cyanogenic plants

HCN has high affinity for Fe in cytochrome oxidase, prevents cellular respiration, causes death

how chronic cyanide poisoning occurs

ingestion of low levels of HCN, causing neurotoxicity/goiter

signs of ingestion of cyanogenic plants

takes 10 minutes - hyperventilation, convulsions, shock, coma, resp failure, death, excitability in cattle

onset of clinical signs from cyanogenic plants

PERACUTE (tachypnea/dyspnea), pupils dilate

color of VENOUS blood from cyanogenic plants

BRIGHT CHERRY RED

treatment of cyanogenic plants

VERY RARE, USUALLY FATAL (if okay, use sodium nitrite to convert hemoglobin to methemoglobin, to compete with CN for receptor)

plants containing nitrites

lambs quarter, pigweed, johnson grass

crops containing nitrates

oats, corn, wheat, alfalfa, sugar beet, soybean

conditions increasing nitrate content in plants

rain after drought, temp extremes, lots of cloudiness, frost, excessive nitrate fertilizer

in normal conditions, why does nitrate NOT build up in plants?

stem/leaves convert nitrate to protein as fast as its taken up by the roots

toxic principle of nitritic plants

NO3 (nitrate) which reduces to NO2 (nitrite)

what does nitrite do?

oxides Hb into MetHb

MoA of nitric plants

nitrite combines with Hb and oxidizes it to MetHb, reducing blood O2 carrying capacity

primary signs of nitrate intoxication

hypoxia, tachypnea, cyanosis, rapid HR, tremors, weakness, coma/convulsions, death

blood color with nitrate poisoning

CHOCOLATE BROWN

treatment of nitrite toxicity

methylene blue, feed low nitrate hay, keep environment quiet

how does methylene blue treat nitrate toxicity?

converts MetHb to Hb, restoring O2 carrying capacity

what species can be poisoned by red maple?

horses and camelids

acer rubrum

red maple

what do red maple leaves cause?

fatal methemoglobinemia and acute hemolytic anemia

toxins from red maples

gallic acid, pyrogallol, tannins

signs of red maple toxicity

rapid HR, tremors, weakness, coma/convulsions, death

why should we NOT use methelyne blue for red maple toxicity

Heinz body anemia may be present, can worsen condition

blood color with red maple poisoning

CHOCOLATE BROWN