lecture 10- toxicants affecting the cardiac and respiratory systems- 2

solanaceae

toxic principle of solanaceae

hyoscyamine

scopolamine

atropine

toxicokinetics of solanaceae

Alkaloids absorbed from the GI tract. Dried seeds in feed and

fresh plant are both sources.

mechanism of toxicity

most of the symptoms can be related to inhibition of the PNS; occur within minutes to several hours

death camas

when does death camas poisoning typically occur

in early spring

toxic agent of death camas

zigacine

clinical signs of death camas

vasodilation and bradycardia, cardiac necrosis; often CNS involvement

white snakeroot

toxic principle of white snakeroot

tremetol and tremetone

toxicokinetics of white snakeroot

tremetone must be activated by microsomal enzyme to produce toxicity toxic agents are found in milk

pumping apparatus function

regulate gas exchange between environment and airways

components of pumping apparatus

respiratory muscles, CNS, chemo/ mechano- receptors

gas exchange unit function

regulate gas exchange between airways and blood

components of gas exchange unit

airways, alveoli, vascilature, fibrous network

airway reactivity

irritant stimulated bronchoconstriction

pulmonary edema

acute lung injury

cardigenic lung edema is demostrated by a case of

fatal taxus poisoning in horses

high levels of fumonisin may cause

fatal pulmonary edema in pigs 1-4 hours after exposure

chlorine/chloramine

irritating to upper airways peak symptoms at 30-90 minutes

in dilte aqueous solutions chloramine is prepared by

the reaction of ammonia with sodium hypochlorite

what does ammonia do

irritates eyes and respiratory membranes, increases the incidence and intensity of microbial or parasitic infections and reduces growth rate

in humans what are the different percents of carbon dioxide and what it causes

In humans, 3% CO-Hb is considered normal; 6–8% causes drifting of attention; 10–20%

headaches; 20–30% dizziness; 30–60% tachypnea, tachycardia and confusion; and 60% fatality.

methane exposure hazard

10-15%

hydrogen sulfide greatest danger

ability to paralyze the respiratory tract

what does overheating frying pans do to birds

pulmonary edema and hemorrhages

poison hemlock toxic principle

pyridine alkaloids, N- methyl coniine, coniine

mechanism of toxicity for poison hemlock

block neuromuscular junction

toxic principle of water hemlock

cicutoxin

mechanism of toxicity for water hemlock

central neuronal inhibition of GABAergic receptors

inhibition from water hemlock results in

seizures culminating in respiratory failure

when does ABPEE typically occur

in the fall 5-10 days after change to a better often lush pasture

what is metabolized to cause ABPEE

L-tryptophan

what plant causes the most cattle death in tennessee

perilla mint

toxic principle of perilla mint

perilla ketone

perilla mint on sweet potatoes

mechanism of toxicity of perilla mint

damage to the pulmonary endothelium and type I pneumocytes resulting in a proliferation of type II pneumocytes

clinical signs of perilla mint

ingestion causes ABPEE

examples of cyanogenic plants

wild cherry, choke cherry, apricot, peach, apple

Johnson grass, arrow grass, Sudan grass

cynogenic plant toxic principle

amygdalin and prunasin

cyanogenic plants toxicokinetics

readily converted to HCN in the GI tract and absorbed

mechanism of toxicity for cyanogenic plants

HCN has a high affinity for Fe3+ preventing cellular respiration and thereby causing death.

in cytochrome oxidase poisoning from ingestion of low levels of HCN may cause neurotoxicity and may even be goitrogenic.

clinical signs of cyanogenic plants

hyperventiliation, convulsions, shock, coma, respiratory failure and death

onset is peracute

venous blood a bright cherry red

cyanogenic plant treatment

Administering sodium nitrite converts some hemoglobin to methemoglobin,which competes with

cytochrome oxidase for CN forming cyanomethemaglobin.

Sodium thiosulfate, in the presence of the enzyme rhodanese, combines rapidly with the CN molecule cleaved

from cyanomethemaglobin to form non-toxic sodium thiocyanate which is excreted in the urine.

plants containing nitrates

Redroot pigweed

lamb’s-quarters

Johnson grass

Sudan grass

sorrel

dock

crops containing nitrates

oats

corn

wheat

alfalfa

sugar beet

soybean

conditions causing increased nitrate content

• drought followed by rain

• extremes of temperature

• extended cloudy conditions

• frost

• excessive nitrate fertilizer rapid growth

toxic principles of nitrates

NO3 which is reduced to NO2

mechanism of toxicity

nitrite combines with hemoglobin and oxidizes it to methemoglobin

diagnosis of nitrates poisoning

treatment of nitrate tox

remove animals from source and fed a low nitrate feed (hay) maintain a quiet environment. use methylene blue

acer rubrum

is a deciduous tree native to northeastern North America. Also

sugar maple, silver maple.

what disease can acer rubrum cause

methemoglobinemia

diagnosis of red maple toxicosis

rapid heart rate, tremors, weakness, coma/ convulsions and death follows within several hours if untreated