Exam 2 Flashcards
(43 cards)
What plant causes these symptoms: “Red as a beet, dry as a bone, blind as a bat, mad as a hatter, and hot as a hare”
What is the toxic agent & type of effects mediated?
Mechanism of action?
Why might an animal avoid eating this plant?
T/F: the seeds are the only toxic part of the plant
Jimsonweeds
Tropane alkaloids - parasympatholytic: increased peripheral vasodilation, blocking of sweating mechanism, decreased salivation, lack of sweating, loss of body temp regulation
Competitive antagonism of central & peripheral muscarinic acetylcholine receptors - inhibition of rest & digest responses
Plant has an unpleasant smell & bitter taste
False: all plant parts are toxic, seeds are most toxic
How might you be able to identify a case of Jimsonweed toxicity postmortem?
Treatment/Management?
Why would a parasympathetic drug (pilocarpine) be possible contraindicated?
Plant material may be present in GI tract
Tx/Mx: Benzodiazepines & barbiturates to control convulsions, supportive care
amount of drug needed to reverse effects would require a toxic amount to the animal & can also suppress breathing
What plants can cause “walking disease” & “stargazing”, ?
Toxic agent of these plants?
What organs are affected?
When do these plants become more toxic?
Senecio spp. & Crotolaria spp.
Pyrrolizidine Alkaloids
Liver (most common), kidney, heart, lung
Drought conditions –> stress
What needs to happen for the pyrrolizidine alkaloids to become effectively toxic to the animal that ingested it?
Mechanism of action?
What risks are we concerned about with chronic exposure?
What drug would result in a lethal toxicity if combined with pyrrolizidine alkaloids?
Metabolized to more active form in the liver –> pyrroles
Pyrroles act as alkylating agents resulting in DNA damage
Carcinogenic effects
Acetaminophen
Acute signs of pyrrolizidine alkaloid toxicity?
T/F: signs of toxicity may take weeks to manifest
What other signs unique to horses are seen in Crotolaria toxicity?
Acute: liver failure (anorexia, behavioral changes, icterus, visceral edema, ascites, photosensitization), sudden death
Chronic: weight loss, behavioral changes (walking disease, stargazing), frequent urination, rectal prolapse
True
Fibrosing alveolitis, laminitis
What postmortem lesions may be seen grossly with Senecio & Crotolaria poisoning?
Histopathologic lesions?
Tx?
Gross: Congested & edematous liver, fibrosis, cirrhosis in chronic cases, icterus, SC & serosal petechiation, edema of lungs & abomasal folds
Histo: centrilobular hepatic degeneration & necrosis, fibrosis, cirrhosis (chronic cases)
Tx: supportive, prevent further feed contamination, avoid exposure of young animals, control plants in pasture
What plant(s) contains taxine alkaloids and can cause sudden death due to heart failure?
Does this toxic agent have a high or low LD50?
T/F: plant is no longer toxic when dried
Mechanism of action?
Taxus spp.,
Low, only need 0.5% of BW of plant material
False
Inhibition of Ca & Na currents across cardiac muscle membranes - slows ventricular muscle contraction
When would you suspect taxine alkaloid toxicity?
How might you diagnose this toxicity postmortem?
Tx?
Sudden death in animals with recent exposure to garden clippings, or signs consistent with heart failure if caught early
Chewed leaves/twigs found in the rumen that resemble rosemary
Tx: avoid disturbance & handling, rumenotomy & AC
Which toxic agents can be found in common household vegetables & cause a Heinz body anemia?
Mechanism of action?
How may this result in abortion?
Gross lesions?
Tx?
Propyl disulfide & dimethyl disulfide (Allium-onion/garlic, Brassica-mustard)
MoA: normally reduced by glutathione, but if glutathione is depleted –> oxygen free radical formation –> hemolysis –> methemoglobinemia
Abortion: fetal hypoxia due to methemoglobin formation
Gross: congested, red-brown spleen & kidneys, pale or icteric carcass
Tx: supportive, diuretics, oxygen,
What is the toxic agent in Euphorbia spp.? Main irritant of the plant?
Effects/MoA?
Most common signs in SA?
Signs in LA?
Tx:
Why would washing the skin with water or milk be contraindicated?
Diterpene esters - plant sap
Inflammation & tumor production
SA: Gi irritation: salivation, vomiting, diarrhea
LA: blistering of exposed skin and MM, salivation, diarrhea +/- blood, collapse & death in extreme cases
Tx: supportive, symptomatic - NSAID’s, ABx, topical ointments, fluids,
Toxins are insoluble in water or milk so washing it with those may drive it deeper into skin - use warm soapy water instead
What kind of toxic agent do these plants contain: Sorghum, Johnsongrass, Vetch, elderberry, wild plum, corn, white clover etc.
MoA of toxin release?
What environmental factors can increases toxicity and how?
MoA of toxin itself?
cyanogenic glycoside
MoA: when plant tissue is damaged, it releases HCN
Env: more nitrogen in soil –> more cyanogenic glycoside production, caterpillar infestations can spread cyanogenic glycosides to surrounding vegetation
MoA: cyanide binds iron in cellular cytochrome oxidase –> blocks electron transfer needed for cellular respiration –> Hb cannot release oxygen to tissues –> blood becomes super saturated with oxygen
Signs of cyanogenic glycoside toxicity?
Postmortem findings?
Tx?
sudden death, CNS abnormalities, signs of oxygen starvation, red MM, muscle tremors, convulsions
PM: petechiae, cherry red blood, +/-almond-like odor
Tx: Methylene blue or sodium nitrite which forms cyanmethemoglobin which pulls cyanide from cytochrome oxydase, then treat with sodium thiosulphate which reacts with cyanmethemoglobin to form soluble thiocyanate –> excreted in urine
What is the main toxic agent in Oleander?
MoA?
Low dose effects?
high dose effects?
Cardiac glycosides
MoA: inhibition of Na/K ATP-ase
LD: Gi effects-vomiting, colic, rumen stasis, bloat, diarrhea
HD: bradycardia, ventricular arrhythmias, weakness, ataxia, tremors, posterior paresis, dyspnea, convulsions, coma
Postmortem findings of cardiogenic glycoside toxicity? (gross & histo)
Tx?
Gross: Sub-epicardial hemorrhages, pulmonary edema, may find leaves in the ingesta, ventral edema
Histo: multifocal myocardial inflammation, degeneration, and necrosis, +/- renal tubular lesions
Tx: remove from source, rumenotomy/stomach lavage may be useful if early, AC, digibind ($$$), atropine, propranolol,
Toxic component of sago palms?
Signs?
Tx?
cycasin (hepatotoxic) & neurotoxins, all plant parts are toxic
Signs: diarrhea (often bloody), liver failure, bleeding
Tx: emesis if early, AC (multiple doses), antiemetics, Vit. K, fresh plasma, SAMe, N-acetylcysteine
What kind of tissue does Fluoride toxicity like to affect?
How is fluoride excreted?
Diagnosis?
Developing/remodeling bone (ends of long bones, developing teeth)
Most in urine, some in milk
Feed, mineral, water analysis, biopsies of vertebrae or ribs, urine fluoride within 1-3 wks of exposure, kidney & liver testing post mortem
? pH & ? temperature in the rumen results in increased ammonia generation
? rumen pH promotes NH4 absorption
excessive ? production causes bloat
Why are hindgut fermenters less susceptible to NPN poisoning?
high & high
Increased
NH3
They have 1/3 to 1/4 the capacity of ruminants to convert NPN to ammonia, thus require 3x-4x the NPN in diet to develop a toxicity
NPN acclimation takes ? days that is lost in ? days when no longer being fed high amounts of NPN
What changes to the diet are made in order to promote growth of NPN converting bacteria?
3-4, 1-2
Easily digestible CHO’s and minerals
Initial signs of NPN toxicity?
Signs as it progresses?
Final stages?
Uneasiness, slight bloat, excessive salivation
tremors, tachypnea, tachycardia, stiffness, ataxia
collapse, lateral recumbency, boat, regurgitation, spasms, convulsions, death
Why would NPN poisoning, which forms alkalemic products, result in normal pH or even an acidemia?
NPN forms NH4 –> raises blood pH –> reduction in ability of cells to carry out oxidative phosphorylation & ATP production –> cells switch to lactate production to meet energy needs –> lactate accumulation results in an acidemic effect which brings back pH down from elevated levels to normal levels or below normal (acidemic)
Antemortem ways of diagnosis in cases of NPN poisoning?
Postmortem ways to diagnose NPN poisoning?
What is more reliable, rumen assay or feed assay?
Antemortem: characteristic signs, history of change in feed, high rumen pH, ammonia smell
Postmortem: rumen content assay for ammonia (need to put sample in sealed container & freeze ASAP), feed assay content for high NPN content, bloat line lesion, pulmonary edema & froth/fluid in trachea
Feed assay (rumen assay unreliable as there is rapid breakdown in ruminal contents)
Feed no more than ?% total NPN
NPN should not be more than ? of total nitrogen?
3%
1/3
What is done with poor quality roughage to increase its quality? What 3 things change in the roughage by doing this?
What happens when this same process is done to higher quality material?
Exposed to high levels of ammonia gas
Increases digestibility, crude protein, palatability
Ammonization introduces amino acids which undergo a condensation reaction with sugars in the feed/roughage to form toxic pyrazines & imidazoles
Clinical picture of animals fed high quality feed that was ammoniated?
Why do you need to be worried about the calves in the same herd that has been exposed (even though the calves aren’t eating roughage yet)
What other precautions must you do (in order to protect human health)
Animals go “bonkers” - spontaneous trembling, rapid blinking or ear twitching, ataxia, apparent blindness, tachypnea, frothing at the mouth, urination, defecation –> stampede and run into objects +/- convulsions –> return to normal in 1-3 days
toxins can be passed through milk
discard contaminated milk for a minimum of 3 days AFTER toxic feed has been removed
