Tox- Plants- Eye+Liver

pbhati17's version from 2018-04-02 00:30


Question Answer
what are the 4 plants that can affect the eye?(1) Datura sp. - thorn apple, jimson weed (2) Brugmansia sp. - angel’s trumpet (3) Solandra sp. - chalice vine (4) Solanum sp. - nightshades (tomatoes, potatoes)
(she kinda lumped these together so i did too) What are the toxins in datura species? and what is their main MOA?(1) DATURA has Tropane alkaloids - l-hyoscyamine (atropine), scopolamine (l-hyoscine)... these have ANTIMUSCARINIC effects. (2) SOLANUM sp has what toxins?: solanine and solanidine (glycoalkaloids) (3) BITTERSWEET (a solanum/nightshade) has what toxin? What effects does it have?: has solasodine have saponin-like effects: disrupting cell membranes by detergent actions causing severe gastrointestinal mucosal necrosis
Explain the anticholinergic effects of datura sp- what does it do/what CSs does it causeCompetitive block of the acetylcholine receptor → ↓ salivation, intestinal motility, dilated pupils and tachycardia. Also has Direct irritant effect on the GIT, causing colic, constipation or hemorrhagic diarrhoea. Certain Solanum species might cause CNS effects in cattle, sheep and goats
which animals are pretty resistant to nightshades?Ruminants are resistant to nightshade toxicity - only large amount of ingestion will cause disease
how do datura species affect the eyes? Other systems?Persistent mydriasis, photophobia, Restlessness, irritability, weakness, sinus tachycardia, dryness of mucous membrane, constipation
how might you be able to dx datura tox?Diagnosis – drip of urine of toxicated animals → mydriasis in cats (lol wtf)
(fun review time bc she mentioned it) what are the cardiac glycoside plants?Milkweed, digitalis, oleander
(fun review time bc she mentioned it) red clover toxin?slaframine
(fun review time bc she mentioned it) Na-K ATPase MOA for toxins?these are the cardiac glycosides (milkweed, digitalis, oleander)
(fun review time bc she mentioned it) oxidative damage toxins?onion, red maple
(fun review time bc she mentioned it) treat methemoglobin with what?methylene blue
(fun review time bc she mentioned it) what does ricin do?(from castor bean) inhibits ribosomal production of proteins


Question Answer
1* vs 2* photosensitizationPRIMARY is when you eat a photodynamic plant. SECONDARY is when the liver is damaged so it cant get rid of the chlorophyll, so then you are photosensitive
Sago palm (Cycas sp): what is the toxin? Who does it affect? what does it do?methylazoxymethanol glycosides are HEPATOTOXIC to DOGS AND SMALL RUMIS (dino palm so cray it needs meth twice)
CSs of sago palm ingestion?(Dogs and sm rumis, methylazoxymethanol glycosides, HEPATOTOXIC) periodic episodes of persistent vomiting, Excess salivation, increased water consumption, Anorexia, diarrhea or constipation, icterus*, ↓ platelets, elevated serum bilirubin, hepatic enzymes, BUN , creatinine....causes an ENLARGED, NUTMEG LIVER **This is centrilobular necrosis
effect of sago on liver? with what toxin?methylazoxymethanol glycoside--> centrilobular necrosis.
Lantana sp.: what is the toxin? what are the problems it causes? (moa/pathophys)Toxin: Lantadenes (triterpenoid), they are BIOTRANSFORMED in the liver--> excreted to bile--> damage bile canalicular membranes and microvilli--> block bile flow--> obstructive cholangitis
CSs of lantana ingestions?(LANTADENES (triterpenoid) are the toxin, bioxformed in liver, damage bile ducts to lead to obstructive cholangitis) initial GIT signs (Depression, loss of appetite, decrease in ruminal motility, constipation/ diarrhea), liver related effects are apparent by 2nd to 3rd day--> can see icterus and photosensitization, Elevated serum bilirubin, AST, ALT. Can cause death due to hepatic disease and renal failure. (subacute or chronic= photosensitization).
(prolly dont need to regurg this) pathology youd see with lantana(obstructive cholangitis eventually liver dz) liver swollen, orange colored due to bile staining. Gall bladder – much enlarged with edematous walls. Reddening and edema of gut mucosa. Microscopic – mild to moderate centrilobular necrosis
what toxic plant causes bighead in sheep?Tetradymis sp. aka horsebrush
horsebrush (Tetradymis sp.): what is the toxin/MOA/pathophys?hepatic biotransformation of the toxicant in Tetradymis to tetradymol*--> liver damage--> Causes Inability of liver to clear phylloerythrin (2* photosensitization). This leads to sheep who feed on this to get a swelling of the head when exposed to light
CS/path of horsebrush (tetradymis) tox?(TETRADYMOL is what is created in liver--> cant clear phylloerythrin-->2* photosensitization) Abrupt onset, loss of appetite, lethargy and depression, Photosesnsitization, ↑ in serum AST, ALT (lol just signs of liver damage). Liver (enlarged/tan), gall bladder distended with bile-- centrilobular hepatic necrosis
what 2 things so far cause centrilobular hepatic necrosis?horsebrush(tetradymis), and sago palm(cycas- with methylazoxymethanol glycoside)
what thing causes inhibiton of oxidative phosphorylation in the mitochondria?cockleburr (xanthium) --- (imagine mitochondria like little burrs)
cockleburr (Xanthium sp.): what is the toxin, what problems does it cause?toxin Carboxyatractyloside (CAT) in seeds within bur and two leaf seedling stage, causes Inhibition of oxidative phosphorylation in mitochondria. So you will see (in pigs and also calves): abrupt onset of signs, depression, weakness, loss of appetite, vomiting, hypothermia, ataxia, spasmodic muscular activity, recumbency and death (see protein rich effusions, liver has centrolobular necrosis)
how can you help tx/prevent cockleburr(xanthium) tox?Parenteral glucose; milk/lard – protective in pigs


Question Answer
WHAT ARE THE Pyrrolizidine alakloid PLANTS?Senecio, Crotalaria, Cynoglossum sp
Crotolaria sp.(rattlebox)-- WHAT ARE THE TOXINS?PYRROLIZIDINE ALKALOIDS!! (in this case for crolatria, monocrotaline specifically) bitch you should know this by now
explain MOA of pyrrolizidine alkaloidsAlkaloids metabolized in liver to highly reactive pyrroles which alkylate DNA ---> alters RNA synthesis--> impair cell division. So the cells grow but are unable to divide --> HEPATOCYTOMEGALY AND KARYOMEGALY
CSs of ingestion of crotalaria?Anorexia, weight loss, Ataxia, icterus, stupor, severe weakness, in HORSES: appear sleepy, drag rear legs when walking, Restless, self mutilation, persistent walking/circling, leaning against solid objects (alkylating DNA means although there is liver damage there can be some neuro stuff too) Cattle - similar signs, depression, excess salivation, ataxia, bloat, icterus, tenesmus with partial eversion of rectum, diarrhea (tar-like)
what will path of crolataria look like? Liver – firm, slightly shrunken, grayish blue, yellow or tan, mottled with irregular reddish brown foci (nutmeg liver). Microscopic: hepatic necrosis, inter/intralobular fibrois, bile duct proliferation, hepatocellular megalocytosis, karyomegaly, central vein fibrois
what stuff in the liver bioactivates the pyrrolizidine alkaloids, what are they metabolized to?mixed function oxidases, hydrolysis and dehydrogenation --> pyrrole metabolites
two words to describe the effect of the pyrrole metabolites when they bind to and cross-link DNA, proteins, amino acids and glutathione (they are potent electrophiles)Effects are cytotoxic and antimitotic
Senecio sp. (Ragwort/groundsel) who are most sensitive to this plant? what is the toxin? what part is most toxic?Contain pyrrolizidine alkaloids with varying potency (highest concentrations in seeds and flowers) - senecionine-- PIGS most sensitive. (can readily cross placenta)
explain the pathology/progressive toxicity of Pyrrolizidine alkaloids*remember they are metabolized to pyrroles in the liver, and these bind and cross link DNA (alter RNA synth and impair cell division) Dose-dependent hepatocyte swelling followed by cellular degeneration, loss of homeostasis and necrosis: acute hepatocellular necrosis, chronic hepatic fibrosis and biliary proliferation.
how does acute vs chronic pyrrolizidine alkaloid tox differ?ACUTE: anorexia, depression, icterus, visceral oedema and ascites, elevation of liver enzymes (AST, ALK, GGT), bili, and bile acids. CHRONIC: slow accumulation of PAs and transient increase in liver enzymes. Liver biopsies will show focal hepatic necrosis or piecemeal necrosis; megalocytes. Often slow progression of the disease: hepatic cripples. Will develop clinical liver failure, photosensitivity when put to physiologic stresses (pregnancy or lactation)
what causes "hepatic cripples"?pyrrolizidine alkaloids in chronic term
Cynoglossum sp. (hounds tongue) what toxin? CS?THIS IS ANOTHER pyrrolizidine alkaloid!! heliosupine is this one. CS: Poor body condition, weight loss, icterus, Head pressing, aimless pacing, ataxia, chewing, yawning, intermittent drowsiness, tenesmus, constipation/diarrhea (path and tx same as for crotalaria)