Tox- Plants- Nervous System 1

pbhati17's version from 2018-04-02 00:31

Nero Tox 1

Question Answer
buckeye (Aesculus sp.) (aka Horse-chestnut; red buckeye; white buckeye) what are the toxins in this? What are the CSs caused by them?TOXINS: saponins, alkaloids. you will see Saw-horse stance, stagger, trembling, hyperesthesia, Seizures with extensor rigidity, collapse.
Locoweed (Astragalus sp.): what are the toxins in this plant? what do the toxins do? (Moa/pathophys)has the alkaloid swainsonine ( induce the classical neurological and pathological signs of locoism= induces neuronal degeneration) but also contains nitro-toxins, and accumulates large amounts of selenium (is a "selenophyte" and can be used as an indicator plant). Usually see effects after chronic ingestion for weeks- inhibits the enzyme α-mannosidase which causes an accumulation of oligosaccharides leading to a pseudo "lysosomal storage disease"
clinical signs you might see with locoweed intoxication?(REMEMER: swainsonine= neuronal degen, and inhibits α-mannosidase which causes accumulation of oligosaccharides to mimic a lysosomal storage dz) HORSES: can get more excitatory signs than other sp. can see ataxia and incoordination. depression, stand with head and neck down as if asleep, stare as if blind . feeding (slow & difficulty in chewing), When handled → violent, maniacal with restraint, they may rear up and fall backwards. OTHER SP: belligerent (comparatively less violent), Weakness, depression, rough hair coat, weight loss, ataxia, solitary
2 things that have toxic nitro-compounds?locoweed, milkvetch (THESE ARE BOTH ASTRAGALUS SP) (these nitro things like to inhibit enzymes-- loco inhibits alpha-mannosidase ((pseudostorage dz), and milkvetch inhibits succinate dehydrogenase (dec energy avail to brain)
milkvetch (Astragalus sp.): what is the toxin? what problem does it cause?3-nitropropionic acid and 3-nitropropanol (miserotoxin). Causes irreversible inhibition of mitochondrial succinate dehydrogenase→ ↓ energy available in brain.
CS/path of milkvetch (astragalus) tox?(miserotoxin= 3-nitropropionic acid and 3-nitropropanol--> Irreversible inhibition of mitochondrial succinate dehydrogenase → ↓ energy available in brain). Abrupt onset → ataxia, recumbency. More gradual onset → weakness, dazed and docile. Difficult in breathing, wheezing, coughing, clicking sound when dewclaw or hooves strike opposite rear leg. Will see foci of necrosis in brain
crazyweed (Oxytropis sp) what are the toxins in this? MOA/pathophys?MOA/toxin Same as locoism (Astragalus sp.): Indolizidine alkaloids (swainsonine), causes Competitive inhibition of α-mannosidase → cannot breakdown mannose containing oligosaccharides (accumulation of oligosaccharides)--- leads to Depression, weight loss, stiff gait, exaggerated limb mvt, anorexia, Violent response to handling or confinement.
*what is milk madness? what causes this/what plants?it is LOCOISM (astragalus sp: locoweed, crazyweed (oxytropis) ) which has the toxins (swainsonine) transferred from dams milk to bb--> EVEN IF THEY RECOVER, NOT GOOD TO RIDE (swainsonine causes neuronal degeneration soooo prolly dont wanna ride this horse)


Question Answer
Golden chain tree (Laburnum sp.): what is the toxin, what is it's MOA?Leaves, legumes & seeds are toxic and contain cytisine alkaloid which is a nicotinic receptor agonist (INC CONTRACTION, INC EXCITABILITY) so this leads to mild-mod neuro dysfunction
CSs of golden chain tree (laburnum)?((REMEMBER IT HAS CYSTINE ALKALOID-->NICOTINIC AGONIST-->inc excitement and neuro dysfunction= INC SLUDGE) increased salivation, anorexia, tremors, colic, Cattle: knuckling of fetlocks, Dogs: abdominal pain, vomiting without diarrhea (AUGHH THAT PICTURE OF KNUCKLING OF FETLOCKS)
*sooo what toxin/plant caused that horrible picture of knuckling of fetlocks on cows?golden chain tree (laburnum)= cystine alkaloid (nicotinic agonist)
Pea (Lathyrus sp)-- what are the two major syndromes/systems affected by peas (lathyrism)?(1) Neurolathyrism (neuro problems) (2) Angiolathyrism
what plant causes Angiolathyrism and neurolathyrism?PEA (LATHYRUS sp)
what are the 3 neuro syndromes which compose neurolathyrism?(1) acute to subacute, sometimes lethal disease, distinctive neuropathologic changes (2) acute often lethal disease without distinctive neuropathologic changes (3) acute → generally non-lethal
what plant causes spastic paresis in humans?PEA (LATHYRUS sp)
Pea (Lathyrus sp): What is the toxin/MOA of toxin-- FOR THE NEUROLATHYRISM? FOR THE ANGIOLATHYRISM?(1) NEURO: contains aminoacids → agonists at central glutamate - kainate and quisqualate excitatory receptors. (2) ANGIOLATHYRISM: induced by aminopropionitrile, this inhibits lysyl oxidase → decrease cross linking of collagen (hence aneurysm)
angiolathyrism-- caused by what plant, it mainly causes _________ in who?dissecting aneurisms in poultry (induced by aminopropionitrile--> inhibits lysyl oxidase → decrease cross linking of collagen)
so when she says pea/lathyrus sp, what are some of the common names for the toxic sp?caley pea, wild winter pea, everlasting pea
CSs of pea intoxicity? for HORSE? SHEEP? CATTLE? CHICKEN?(remember-- neurolathyrism=Aminoacid that is agonist at central glutamate receptor. For angiolathyrism=aminopropionitrile, which inhibits **lysyl oxidase and dec collagen cross linking) HORSE: stiff gait, hyperexcitable, weak, struggle to stand, flaccid paraplegia, paresis or paralysis of larynx with roaring (will see degeneration of motor neurons brain stem, medulla, spinal tracts, focal demyelination, laryngeal nerve demyelination) SHEEP: abrupt onset, lethargy, anorexia, pacing, head pressing, increase salivation, grinding of teeth. CATTLE: (as sheep) – paraplegia, lameness, stand hunched-up legs under body, prefer to lie down, muscular tremors. CHICKEN: DISSECTING ANURYSM


Question Answer
how does brackenfern cause ataxia and incoordination in horses? tx?(MOA: (1) ptaquiloside forms pterosine B that alkylates purine bases in DNA- BM suppression. (2) activates oncogenes (H-ras proto-oncogene) in GI/UT --> bovine enzootic hematuria (3) has thiaminase 1 and 2 which break down thiamine.) FOR NEURO SIGNS, ITS BECAUSE OF THE THIAMINASE--> LACK OF THIAMINE LEADS TO PEM (polioencephalomalacia) and this leads to... depression, ataxia, unable to stand, marked loss of body condition, muscular twitching, causing jerky movements of head, neck, limbs, tail. TX BY GIVING THIAMINE (B1) parenterally
**what causes "Crazy cow"?Solanum/nightshade
how does Solanum (nightshade) cause ataxia and incoordination/"crazy cow"? CS? How do you test if they have crazy cow?(nightshades have many diff toxins: (1) Tropane alkaloids(atropine, scopalamine) for datura sp= ANTIMUSCARINIC EFFECTS. (2) glycoalkaloids (solanine and solanidine) for solanum species= anticholinergic, CNS stuff. (3) solasodine (saponin-like effects) for bittersweet= GI mucosal necrosis bc disrupts cell membrane with detergent like effect)--- so, see "crazy cow" with: tremors, ataxia, collapse, nystagmus, struggle to stand, able to rise after brief rest. TEST: raising and twisting head for 1 minute & with sudden release of head → collapse
Cannabis sativa: What are the toxins? what is the MOA of them? Contains several cannabinoidsdelta-9-tetrahydrocannabinol (THC) is the most important. Binds to cannabinoid receptor (CB1) which leads to effects in both the: (1) CNS: cognitive functions, emotional status, dopaminergic signaling (2) ANS (autonomic nervous system) pain perception and cardiovascular and gastrointestinal function...... AND THEN it also binds to CB2 receptors, leading to changes in inflammation and pain regulation
CSs of cannabis intoxication?(remember that cannabinoids, esp THC, bind to CB1 and CB2 receptors causing changes in the CNS and ANS) Depression, drowsiness, Interspersed periods – arousal, bizarre actions, hyperactivity, tremors, hyper-responsiveness to touch and sound, Appear glassy-eyed, dizzy or disoriented, Decreased body temperature, saw-horse stance, Diarrhea & vomiting in dogs, cats prone to excitement, Recovery in few hours to 4 days
larkspur (Delphinium sp): What is the toxin/MOA for this?Diterpenoid alkaloids (methyllcaconitine) → curare like competitive neuromuscular blocking effects → inhibit acetylcholine at nicotinic postsynaptic receptor sites--> Nondepolarizing neuromuscular blockade → loss of motor function particularly of diaphragm and esophagus
when is larkspur most toxic? Who is suseptible?Rumis and horses (horses lower risk), Risk mainly at flowering and early fruit formation (when plants are both toxic and palatable)
CSs of larkspur? (delphinium)(remember its toxin of alkaloid origin (methyllcaconitine <--last part kinda looks like nicotine, and it works on nicotinic mm receptors) causes CURARE LIKE COMPETITIVE NM BLOCKADE --> non-depol nm blockade) So see: Abrupt onset of episodic weakness, uneasiness, wide-stranded legged stance, rests, rises and falls again, paresis, paralysis/muscle weakness, recumbency. Bloat especially when animal is lying facing down, Respiratory difficulties – death due to respiratory failure, complicated by bloat
how does larkspur cause death?non-depol nm blockage via curare like competition means RESP FAILURE (paralyzed diaphragm) and RECUMBENCY--> BLOAT (imagine a lark flying into a cow's diaphragm repeatedly to stab it with curare)