Cherry (Prunus sp.)/ other stone fruits: What are the toxic compounds? How do these toxins become active?
cyanogenic glycosides in the cell → released after chewing. Amygdalin in the seeds, Prunasin found in leaves, bark and shoots.Glycosides are metabolised by glycosidases into cyanide
what is the MOA of cyanide tox? Which plants have these toxins again?
(CHERRY/OTHER STONE FRUITS have cyanogenic glycosides (amygdalin, prunasin) which are metabolized by glycosidases into CYANIDE). What cyanide does is it inhibits mitochondrial cytochrome c oxidase ((enzyme ESSENTIAL FOR CARRYING OUT CELLULAR RESPIRATION)--> inhibiting cellular respiration. Because of this, hgb cannot release O2--> SUPERSATURATION of the blood with oxyhemoglobin ((lol so cherries make your blood cherry red. nice. then just associate it with other stone fruits, Cyanide (pretty sure its common knowledge pits have cyanide) and that the cyanide comes from cyanogenic gycosides
clinical signs of cherry poisoning?
(cyanogenic glycosides (amygdalin/prunasin)--> glycosidases--> cyanide--> inhibit mitochondrial cytochrome c oxidase--> Hgb cant let go of O2--> supersaturation of oxyhgb) Usually presents as sudden death in a variety of animals, due to rapid development of respiratory failure. Necropsy findings are nonspecific and include slow blood coagulation, generalised congestion and centrilobular liver necrosis due to hypoxia
what can you use to treat cherry poisoning?
(remember its supersat of oxyhemoglobin) Usually too fast progression to tx, but if you can: sodium thiosulfate, methylene blue, sodium nitrite and hydroxycobalamin can be used
alfalfa, lucerne (Medicago sp): what is the toxin and its MOA for this? Who does it affect most?
Mostly affects RUMIS. Eating these overloads the rumen with TRYPTOPHAN. The bacteria in the rumen convert the tryptophan to 3 methylindole--> this is absorbed into the blood and metabolized in the lung to ultimate toxin. This toxin causes Acute pneumonia like signs, febrile condition (toxic to alveolar cells and bronchiolar cells)
CS/effect on body of alfalfa/lucerne (medicago)
(REMEMBER has tryptophan-->microbes convert to 3 methylindole--> lung enzymes convert it to ULTIMATE TOXIN--> is toxic to alveolar cells and bronchiolar cells) see: Abrupt onset, labored respiration, loud expiratory grunts, open-mouth breathing, frothy salivation, death. ((lungs are full of edema, are pneumonic, emphysema in CT)
what has "ultimate toxin", what does it do?
its from ALFALFA/LUCERNE (they contain tryptophan-->microbes turn to 3-methylindole-->lungs to ultimate toxin) cause lung damage (edema, penumonia, bronchitis)
Purple mint (Perilla sp.): what is the toxin, what problem does this cause (in who?)?
Produces ARDS signs (acute resp distress syndrome) aka "panting dz" which happens in late summer/early fall for cattle. This is bc it has Volatile, aromatic 3-substituted furan ketones which cause excessive proliferation of type II pneumocytes, glandular appearance of tissue (type one is what deals with oxygenating so uh this is a big deal)
what is associated with ARDS/panting dz? why is there panting?
PURPLE MINT, because it has Volatile, aromatic 3-substituted furan ketones which turn type 1 pneumocytes into type 2. (I'm pretty FURious that this mint is so strong i can barely breathe)
Bull nettle & stinging nettle: what problems do these cause, what can you do about it?
these cause irritant effects and you will see erythema, blisters, pruritus, swelling. With dogs you will see them salivate profusely, lick paws, scratch at nose, face and other body areas, retch and vomit. TX: NSAIDs (dec inflamamtion)
pigweed (Amaranthus sp.): how is this plant toxic?
TOXIN UNKNOWN, BUT CAUSES NEPHROTOXICITY. Death can occur due to 2* hyperkalemia leading to cardiac dysfunction (kidney not working, NaK pump not working...losing salt and retaining K) this plant ALSO accumulates nitrate if it is stressed, and if the animal eats it, it can lead to nitrate toxicosis (remember that pearl millet, sorgum, and sudan also cause nitrate tox. Remember that rumen converts nitrates to nitrites, nitrites oxidize the Fe in Hgb, which makes methemoglobin--> cant carry O2 properly)
CSs of pigweed (amaranthus) tox?
(REMEMBER. pigweed has known nephrotoxic toxin. So see kidney failure and probs related to that. Also can have high nitrate levels which risk methemoglobin formation)) Onset over 1-2 days, weakness, trembling, ataxia, recumbency, flaccid paralysis , coma & death, ↑ urination, inc BUN, inc K+. Kidneys will have renal tubular epithelial necrosis with the prox tubules dilated and full of proteinaceous material.
Oak trees (Quercus sp.) what are the toxic principles, where/when are they most toxic? What are the effects and what will you see?
NEW SPRING GROWTH has high conc of toxic compounds: gallotannins, tannic acid, pyrogallol and phenolic acid. These tannins and related compounds are astringents and and they denature cell proteins. You will see transient elim of red or brown urine.
CSs of oak tox?
(remember, high in tannins and related compounds which are astringent and denature cell proteins) see: cattle become more depressed, can show abdominal pain, nasal discharge, PU/PD, increased respiratory rate. LAter is diarrhoea (possibly bloody), dehydration, colic, edema, weakness and sometimes icterus (see elevated BUN, AST, SDH, hypocalcemia, hyperphosphatemia)
Halogeton: what are the CSs of halogeton tox? who is most affected?
(WIKI SAYS: toxic bc high amounts of sodium oxalate) Sheep – dull, loss of appetite, drooling of saliva... Later: increase in severity, weak/stiff muscles, irreg respiration, Decrease in blood calcium; increased urination. You will see a fluid filled abd cavity, kidneys will be pale and full of crystals, renal tubular epithelial necrosis, proximal tubules dilated with proteinaceous material and oxalate crystals
how do you tx halogeton tox?
Ca supplementation!!! Bc the toxic principal (NaOxalate) chelates Ca++
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