Toxic Principles in Plants Flashcards
MOA of insoluble calcium oxalate?
plant cells have needle shaped calcium oxalate crystals that penetrate the oral mucosa and tongue
Clinical signs of insoluble calcium oxalate?
irritation of lips, mouth, throat, V+, some cases die of suffocation
MOA of soluble calcium oxalate?
bind to Ca and precipitation of insoluble calcium oxalates in soft tissues and kidney
Clinical signs of soluble calcium oxalate?
hypocalcemia, kidney damage
MOA of isocupressic acid?
vasoconstriction and decrease in uterine blood flow–increased fetal cortisol levels
Clinical signs of isocupressic acid?
abortion in cattle
MOA of quinone?
primary photosensitization
Clinical signs of quinone?
erythema and pruritus, edema, and necrosis of skin–secondary bacterial infections
MOA of tannic acid?
tissue damage including GI lesions and kidney damage
Clinical signs of tannic acid?
cattle–>constipation, brown urine, atony, anorexia, depression
monogastrics–>mainly GI
MOA of triterpene acid?
liver damage and hepatic photosensitization
Clinical signs of triterpene acid?
depression, anorexia, constipation, diarrhea, icterus, photophobia, erythema of skin, swelling, necrosis and sloughing
MOA of colchicine?
anti mitotic by binding to tubular and inhibiting spindle formation during cell division
Clinical signs of colchicine?
involves many organs
MOA of diterpene alkaloids?
Competitive blockade of the nicotinic receptors at the muscle endplate similar to curare
Clinical signs of diterpene alkaloids?
- sudden death in cattle
- Early signs are signs of neuromuscular blockade including muscle weakness, stiffness, staggering, bloating, recumbency, and collapse
- Monkshood also show cardiac arrhythmias
Treatment for diterpene alkaloid toxicosis?
antidote is physostigmine or neostigmine
MOA and clinical signs of ergot alkaloids?
vasoconstriction and gangrene, uterine contraction
MOA of indolizidine alkaloids?
inhibition of lysosomal enzymes (decreased glycoproteins), peripheral neuronal degeneration (via nitropropanol glycoside also found in plants), abnormal hoof and hair (via selenium also found in plants)
Clinical signs of indolizidine alkaloids?
neuronal signs; depression, incoordination, ataxia, circling, abnormal behavior
infertility, congenital defects, heart failure, wt. loss, dec immune
MOA of lycorine?
emetic and purgative–bulb is most toxic
Clinical signs of lycorine?
anorexia, salivation, V+, D+, hypotension, muscle tremors/seizures
MOA of muscarine?
stimulation of muscarinic cholinergic receptors
Treatment of muscarine?
antidote is atropine, symptomatic tx and decontamination
MOA of piperidine alkaloids?
nicotinic effects starting w/ ganglionic and neuromuscular stimulation followed by ganglionic and neuromuscular blockade
Clinical signs of piperidine alkaloids?
ataxia, incoordination, birth defects (skeletal malformation and cleft palate)
MOA of pyridine alkaloids (nicotine and lobeline)?
Nicotine and lobeline act on nicotinic receptors at autonomic ganglia, neuromuscular junction and some synapses in the CNS. low doses cause depolarization. large doses cause blockade
Clinical signs of pyridine alkaloids (nicotine and lobeline)?
- Rapid onset of clinical signs
- Early signs are excitation, salivation, lacrimation, vomiting, diarrhea, and tachypnea
- Muscle twitching, muscle weakness, and dyspnea • Death is due to respiratory failure
MOA of pyrrolizidine alkaloids?
hepatotoxic
MOA of solanine and solanidine alkaloids?
GI, CNS, respiratory, cardiac
MOA of taxine alkaloids?
cardiotoxic and GI
MOA of xanthine alkaloids (caffeine, theophylline, theobromide)?
blocking adenosine (A) receptors, inhibiting phosphodiesterase
Clinical signs of xanthine alkaloids (caffeine, theophylline, theobromide)?
salivation, V+, colic, D+, CNS stimulation, convulsive seizures, muscle tremors, tachycardia, hypotension, urination
MOA of anthraquinone?
purgative
MOA of calcinogenic glycosides (vit D analog)?
hypercalcemia; calcification of elastic tissues of the arteries, tendons and ligaments and increased density of bone
Clinical signs of carcinogenic glycosides (vit D analog)?
lameness
MOA of carboxyatractyloside (sulfated glycoside)?
hepatotoxicity, renal damage, hypoglycemia, excessive salivation
MOA of cardiac glycoside?
cardiotoxic by inhibiting Na/K ATPase
MOA of coumarin glycoside?
form dicoumarol in spoiled plants. inhibit vit K epoxide reductase resulting in deficiency of coag factors 2, 7, 9, 10